nifedipine  (Millipore)


Bioz Verified Symbol Millipore is a verified supplier  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 99
    Name:
    Nifedipine
    Description:

    Catalog Number:
    n114
    Price:
    None
    Applications:
    Refer to the product's Certificate of Analysis for more information on a suitable instrument technique. Contact Technical Service for further support.
    Buy from Supplier


    Structured Review

    Millipore nifedipine
    Nifedipine

    https://www.bioz.com/result/nifedipine/product/Millipore
    Average 99 stars, based on 49 article reviews
    Price from $9.99 to $1999.99
    nifedipine - by Bioz Stars, 2021-01
    99/100 stars

    Images

    1) Product Images from "Sialoglycosylation of RBC in Visceral Leishmaniasis Leads to Enhanced Oxidative Stress, Calpain-Induced Fragmentation of Spectrin and Hemolysis"

    Article Title: Sialoglycosylation of RBC in Visceral Leishmaniasis Leads to Enhanced Oxidative Stress, Calpain-Induced Fragmentation of Spectrin and Hemolysis

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0042361

    Calcium influx into RBC upon sensitization with anti-9- O -AcSGP IgG VL antibodies. For all experiments, erythrocytes were washed and loaded with the Ca 2+ -indicator fluorochrome Fluo-3/AM in Ringer solution. A23187-treated Fluo-3/AM-loaded RBC VL served as positive controls (black line) and A23187-treated cells in the presence of EGTA as negative controls (gray background). A. Fluo-3/AM loaded RBC VL and RBC N (2×10 7 ) were left unsensitized or sensitized with varying concentrations of anti-9- O -AcSGP IgG VL or anti-9- O -AcSGP IgG NHS , respectively, (0–40 µg/ml) in Ringer solution for 30 min at 37°C. After washing the cells twice with same solution the fluorescence intensities of the Ca 2+ . B. Cells treated as in A with 0.5 µg/ml (red line), 1.0 µg/ml (green line) and 2.5 µg/ml (pink line) anti-9- O -AcSGP IgG VL were analyzed by flow cytometry to determine the fraction of responding RBC. C. Similarly, RBC N were analyzed without and with sensitization with 5 µg/ml anti-9-O-AcSGP IgG NHS (blue line). D–E. Time dependent increase of intracellular Ca 2+ in RBC VL after sensitization with anti-9- O -AcSGP IgG VL (2.5 µg/ml) for 5 min (red line), 10 min (green line), 20 min (pink line) and 30 min (blue line) at 37°C. Cells were washed and analyzed by flow cytometry. D. Histogram representation; E. Mean fluorescence intensities calculated from D. F–G. Inhibition of the Ca 2+ influx into RBC sensitized with anti-9- O -AcSGP IgG VL . Prior to sensitization with anti-9- O -AcSGP-IgG VL (2.5 µg/ml), the cells were incubated without (green line) or with the P/Q-type channel blocker ω-agatoxin TK (1 µM, pink line, F ), or without (green line) or with the L-type channel blocker nifedipine (10 µM, blue line, G ) and analyzed by flow cytometry.
    Figure Legend Snippet: Calcium influx into RBC upon sensitization with anti-9- O -AcSGP IgG VL antibodies. For all experiments, erythrocytes were washed and loaded with the Ca 2+ -indicator fluorochrome Fluo-3/AM in Ringer solution. A23187-treated Fluo-3/AM-loaded RBC VL served as positive controls (black line) and A23187-treated cells in the presence of EGTA as negative controls (gray background). A. Fluo-3/AM loaded RBC VL and RBC N (2×10 7 ) were left unsensitized or sensitized with varying concentrations of anti-9- O -AcSGP IgG VL or anti-9- O -AcSGP IgG NHS , respectively, (0–40 µg/ml) in Ringer solution for 30 min at 37°C. After washing the cells twice with same solution the fluorescence intensities of the Ca 2+ . B. Cells treated as in A with 0.5 µg/ml (red line), 1.0 µg/ml (green line) and 2.5 µg/ml (pink line) anti-9- O -AcSGP IgG VL were analyzed by flow cytometry to determine the fraction of responding RBC. C. Similarly, RBC N were analyzed without and with sensitization with 5 µg/ml anti-9-O-AcSGP IgG NHS (blue line). D–E. Time dependent increase of intracellular Ca 2+ in RBC VL after sensitization with anti-9- O -AcSGP IgG VL (2.5 µg/ml) for 5 min (red line), 10 min (green line), 20 min (pink line) and 30 min (blue line) at 37°C. Cells were washed and analyzed by flow cytometry. D. Histogram representation; E. Mean fluorescence intensities calculated from D. F–G. Inhibition of the Ca 2+ influx into RBC sensitized with anti-9- O -AcSGP IgG VL . Prior to sensitization with anti-9- O -AcSGP-IgG VL (2.5 µg/ml), the cells were incubated without (green line) or with the P/Q-type channel blocker ω-agatoxin TK (1 µM, pink line, F ), or without (green line) or with the L-type channel blocker nifedipine (10 µM, blue line, G ) and analyzed by flow cytometry.

    Techniques Used: Fluorescence, Flow Cytometry, Cytometry, Inhibition, Incubation

    2) Product Images from "Nifedipine improves blood flow and oxygen supply, but not steady-state oxygenation of tumours in perfusion pressure-controlled isolated limb perfusion"

    Article Title: Nifedipine improves blood flow and oxygen supply, but not steady-state oxygenation of tumours in perfusion pressure-controlled isolated limb perfusion

    Journal: British Journal of Cancer

    doi: 10.1038/sj.bjc.6600611

    ( A ) RBC-flux and ( B ) resistance to flow (TVR) during isolated limb perfusion upon application of nifedipine. Data represent mean±s.e.m. ( n =number of tumours investigated; the RBC flux value of each tumour was obtained by calculating the mean values from up to three individual probes located in central and peripheral regions of the tumour).
    Figure Legend Snippet: ( A ) RBC-flux and ( B ) resistance to flow (TVR) during isolated limb perfusion upon application of nifedipine. Data represent mean±s.e.m. ( n =number of tumours investigated; the RBC flux value of each tumour was obtained by calculating the mean values from up to three individual probes located in central and peripheral regions of the tumour).

    Techniques Used: Flow Cytometry, Isolation

    Changes of mean tumour pO 2 during isolated limb perfusion upon application of nifedipine compared to the pO 2 value immediately prior to the commencement of drug infusion. Data represent mean±s.e.m. ( n =number of tumours investigated).
    Figure Legend Snippet: Changes of mean tumour pO 2 during isolated limb perfusion upon application of nifedipine compared to the pO 2 value immediately prior to the commencement of drug infusion. Data represent mean±s.e.m. ( n =number of tumours investigated).

    Techniques Used: Isolation

    Perfusate flow rate during isolated limb perfusion upon application of nifedipine or vehicle alone (gray bar). Data represent mean±s.e.m. ( n =number of perfusion experiments).
    Figure Legend Snippet: Perfusate flow rate during isolated limb perfusion upon application of nifedipine or vehicle alone (gray bar). Data represent mean±s.e.m. ( n =number of perfusion experiments).

    Techniques Used: Flow Cytometry, Isolation

    3) Product Images from "Striatal proenkephalin gene induction: coordinated regulation by cyclic AMP and calcium pathways"

    Article Title: Striatal proenkephalin gene induction: coordinated regulation by cyclic AMP and calcium pathways

    Journal: Brain research. Molecular brain research

    doi:

    Proenkephalin induction by forskolin is inhibited by the L-type Ca 2+ channel antagonist nifedipine, by the CaMK inhibitor KN62, and by the PKA inhibitor H89. (A) Forskolin (10 μM)-induced expression of the proenkephalin gene is blocked by nifedipine (20 μM). (B) The proenkephalin construct pENKAT12 , transfected into primary striatal neurons, is induced by forskolin (10 μM). The induction is blocked by nifedipine (20 μM). The Δ80 construct is not induced by forskolin. (C) pENKAT12 -induction by forskolin (10 μM) is blocked by KN62 (30 μM), and by H89 (20 μM), (D). Average fold induction of n =7–10±S.E.M. is shown. * P
    Figure Legend Snippet: Proenkephalin induction by forskolin is inhibited by the L-type Ca 2+ channel antagonist nifedipine, by the CaMK inhibitor KN62, and by the PKA inhibitor H89. (A) Forskolin (10 μM)-induced expression of the proenkephalin gene is blocked by nifedipine (20 μM). (B) The proenkephalin construct pENKAT12 , transfected into primary striatal neurons, is induced by forskolin (10 μM). The induction is blocked by nifedipine (20 μM). The Δ80 construct is not induced by forskolin. (C) pENKAT12 -induction by forskolin (10 μM) is blocked by KN62 (30 μM), and by H89 (20 μM), (D). Average fold induction of n =7–10±S.E.M. is shown. * P

    Techniques Used: Expressing, Construct, Transfection

    The L-type Ca 2+ channel agonist FPL 64176 induces proenkephalin synthesis in primary striatal culture. (A) Proenkephalin gene levels are upregulated by the L-type Ca 2+ channel agonist FPL 64176 (20 μM). This upregulation is blocked by the L-type Ca 2+ channel antagonist nifedipine (20 μM). (B) The proenkephalin construct pENKAT12 , transfected into primary striatal neurons, is induced by FPL 64176 (20 μM). The induction is blocked by nifedipine (20 μM). The construct with a shorter promoter, Δ80, is not induced by FPL 64176. Average fold induction of n =4–7±S.E.M. is shown. * P
    Figure Legend Snippet: The L-type Ca 2+ channel agonist FPL 64176 induces proenkephalin synthesis in primary striatal culture. (A) Proenkephalin gene levels are upregulated by the L-type Ca 2+ channel agonist FPL 64176 (20 μM). This upregulation is blocked by the L-type Ca 2+ channel antagonist nifedipine (20 μM). (B) The proenkephalin construct pENKAT12 , transfected into primary striatal neurons, is induced by FPL 64176 (20 μM). The induction is blocked by nifedipine (20 μM). The construct with a shorter promoter, Δ80, is not induced by FPL 64176. Average fold induction of n =4–7±S.E.M. is shown. * P

    Techniques Used: Construct, Transfection

    4) Product Images from "Electrical slow waves in the mouse oviduct are dependent on extracellular and intracellular calcium sources"

    Article Title: Electrical slow waves in the mouse oviduct are dependent on extracellular and intracellular calcium sources

    Journal: American Journal of Physiology - Cell Physiology

    doi: 10.1152/ajpcell.00293.2011

    Effects of the L-type Ca 2+ channel antagonist nifedipine and agonist BAY K8644 on slow wave generation. A : slow wave activity recorded in the absence and presence of nifedipine (1 μM). Nifedipine induced membrane depolarization from −66
    Figure Legend Snippet: Effects of the L-type Ca 2+ channel antagonist nifedipine and agonist BAY K8644 on slow wave generation. A : slow wave activity recorded in the absence and presence of nifedipine (1 μM). Nifedipine induced membrane depolarization from −66

    Techniques Used: Activity Assay

    5) Product Images from "Ghrelin Decreases Firing Activity of Gonadotropin-Releasing Hormone (GnRH) Neurons in an Estrous Cycle and Endocannabinoid Signaling Dependent Manner"

    Article Title: Ghrelin Decreases Firing Activity of Gonadotropin-Releasing Hormone (GnRH) Neurons in an Estrous Cycle and Endocannabinoid Signaling Dependent Manner

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0078178

    Effect of antagonists on the ghrelin-modulated firing activity and resting potential of GnRH neurons in metestrous mice. a ) Block of fast neurotransmission by kynurenic acid (kyn) and picrotoxin (pic) eliminated the action of ghrelin (N=4). b ) The GHS-R antagonist JMV2959 also abolished effect of ghrelin (N=11). c ) Antagonizing the endocannabinoid CB1 receptor by AM251 abolished effect of ghrelin (N=10). d ) Depletion of the intracellular Ca 2+ -pools by thapsigargin (thap) showed no effect on the ghrelin-induced decrease in the firing activity (N=4). e ) Bar graph shows elimination of effect of ghrelin by inhibition of fast neurotransmission, by antagonizing ghrelin receptor or by block of CB1 but not by depleting the intracellular Ca 2+ -sources. f ) Current clamp measurement showed slight depolarization upon ghrelin administration. g ) Depolarizing effect of ghrelin was eliminated by nifedipine. *=p
    Figure Legend Snippet: Effect of antagonists on the ghrelin-modulated firing activity and resting potential of GnRH neurons in metestrous mice. a ) Block of fast neurotransmission by kynurenic acid (kyn) and picrotoxin (pic) eliminated the action of ghrelin (N=4). b ) The GHS-R antagonist JMV2959 also abolished effect of ghrelin (N=11). c ) Antagonizing the endocannabinoid CB1 receptor by AM251 abolished effect of ghrelin (N=10). d ) Depletion of the intracellular Ca 2+ -pools by thapsigargin (thap) showed no effect on the ghrelin-induced decrease in the firing activity (N=4). e ) Bar graph shows elimination of effect of ghrelin by inhibition of fast neurotransmission, by antagonizing ghrelin receptor or by block of CB1 but not by depleting the intracellular Ca 2+ -sources. f ) Current clamp measurement showed slight depolarization upon ghrelin administration. g ) Depolarizing effect of ghrelin was eliminated by nifedipine. *=p

    Techniques Used: Activity Assay, Mouse Assay, Blocking Assay, Inhibition

    6) Product Images from "The bioelectrical basis and validity of gastrointestinal extracellular slow wave recordings"

    Article Title: The bioelectrical basis and validity of gastrointestinal extracellular slow wave recordings

    Journal: The Journal of Physiology

    doi: 10.1113/jphysiol.2013.254292

    Comparison of intestinal slow wave potentials before and after nifedipine administration
    Figure Legend Snippet: Comparison of intestinal slow wave potentials before and after nifedipine administration

    Techniques Used:

    7) Product Images from "Effect of 18β-glycyrrhetinic acid on electromechanical coupling in the guinea-pig renal pelvis and ureter"

    Article Title: Effect of 18β-glycyrrhetinic acid on electromechanical coupling in the guinea-pig renal pelvis and ureter

    Journal: British Journal of Pharmacology

    doi: 10.1038/sj.bjp.0703004

    (A) tracing illustrating the time-dependent effect of 18βGA (30 μM) on the EFS-evoked AP of the guinea-pig ureter. Note that 18βGA abolished the spike component of the AP and reduced contraction. At 30 min from start of superfusion with 18βGA, a bell-shaped AP with long latency was recorded in the presence of 18βGA. Nifedipine 1 μM promptly aboplished the residual electrical and mechanical responses to EFS receorded in the presence of 18βGA. (B) shows the electrical (a) and mechanical (b) responses to EFS measured before and 30 min after addition of 18βGA on an expanded time-scale: note that, in the presence of 18βGA the contractile response to EFS ensued before an electrical event was detectable at this time (see discussion). Calibration bars in A also apply to B.
    Figure Legend Snippet: (A) tracing illustrating the time-dependent effect of 18βGA (30 μM) on the EFS-evoked AP of the guinea-pig ureter. Note that 18βGA abolished the spike component of the AP and reduced contraction. At 30 min from start of superfusion with 18βGA, a bell-shaped AP with long latency was recorded in the presence of 18βGA. Nifedipine 1 μM promptly aboplished the residual electrical and mechanical responses to EFS receorded in the presence of 18βGA. (B) shows the electrical (a) and mechanical (b) responses to EFS measured before and 30 min after addition of 18βGA on an expanded time-scale: note that, in the presence of 18βGA the contractile response to EFS ensued before an electrical event was detectable at this time (see discussion). Calibration bars in A also apply to B.

    Techniques Used:

    8) Product Images from "Differential inhibition of N and P/Q Ca2+ currents by 5-HT1A and 5-HT1D receptors in spinal neurons of Xenopus larvae"

    Article Title: Differential inhibition of N and P/Q Ca2+ currents by 5-HT1A and 5-HT1D receptors in spinal neurons of Xenopus larvae

    Journal: The Journal of Physiology

    doi: 10.1111/j.1469-7793.1998.103bz.x

    Composition of the HVA currents in Xenopus spinal neurons Aa, HVA Ca 2+ current elicited by a test pulse to +20 mV from a holding potential of −50 mV in control, agatoxin (200 nM), ω-CgTx (1 μM) and nifedipine (10 μM). b, time course of block measured at the points indicated in a. B, summary showing that agatoxin blocked 21.8 ± 0.9 % of total HVA current ( n = 24, P/Q-type), ω-CgTx blocked 66.3 ± 1.1 % of total HVA current ( n = 21, N-type), and nifedipine blocked 4.2 ± 0.8 % ( n = 5, L-type).
    Figure Legend Snippet: Composition of the HVA currents in Xenopus spinal neurons Aa, HVA Ca 2+ current elicited by a test pulse to +20 mV from a holding potential of −50 mV in control, agatoxin (200 nM), ω-CgTx (1 μM) and nifedipine (10 μM). b, time course of block measured at the points indicated in a. B, summary showing that agatoxin blocked 21.8 ± 0.9 % of total HVA current ( n = 24, P/Q-type), ω-CgTx blocked 66.3 ± 1.1 % of total HVA current ( n = 21, N-type), and nifedipine blocked 4.2 ± 0.8 % ( n = 5, L-type).

    Techniques Used: Blocking Assay

    9) Product Images from "LTP in hippocampal area CA1 is induced by burst stimulation over a broad frequency range centered around delta"

    Article Title: LTP in hippocampal area CA1 is induced by burst stimulation over a broad frequency range centered around delta

    Journal:

    doi: 10.1101/lm.1179109

    The NMDA receptor antagonist, AP5, altered the postsynaptic response to burst stimulation but did not affect the response during continuous tetanization. The L-type calcium channel antagonist, nifedipine, had no discernible effects on the postsynaptic
    Figure Legend Snippet: The NMDA receptor antagonist, AP5, altered the postsynaptic response to burst stimulation but did not affect the response during continuous tetanization. The L-type calcium channel antagonist, nifedipine, had no discernible effects on the postsynaptic

    Techniques Used:

    10) Product Images from "Uptake, biotransformation and elimination of selected pharmaceuticals in a freshwater invertebrate measured using liquid chromatography tandem mass spectrometry"

    Article Title: Uptake, biotransformation and elimination of selected pharmaceuticals in a freshwater invertebrate measured using liquid chromatography tandem mass spectrometry

    Journal: Chemosphere

    doi: 10.1016/j.chemosphere.2017.05.083

    Toxicokinetic profiles of selected pharmaceuticals in G. pulex measured using LC-MS/MS. Solid line represents model fit, dashed lines represent 95% confidence interval. (a) carbamazepine, (b) diazepam, (c) metoprolol, (d) nifedipine, (e) propranolol, (f) trimethoprim, (g) temazepam and (h) warfarin.
    Figure Legend Snippet: Toxicokinetic profiles of selected pharmaceuticals in G. pulex measured using LC-MS/MS. Solid line represents model fit, dashed lines represent 95% confidence interval. (a) carbamazepine, (b) diazepam, (c) metoprolol, (d) nifedipine, (e) propranolol, (f) trimethoprim, (g) temazepam and (h) warfarin.

    Techniques Used: Liquid Chromatography with Mass Spectroscopy, Mass Spectrometry

    11) Product Images from "Developmental changes in the expression of low-voltage-activated Ca2+ channels in rat visual cortical neurones"

    Article Title: Developmental changes in the expression of low-voltage-activated Ca2+ channels in rat visual cortical neurones

    Journal: The Journal of Physiology

    doi: 10.1111/j.1469-7793.1998.385bn.x

    Steady-state inactivation of LVA Ca 2+ current in P2 neurones A , voltage dependence of steady-state inactivation of the nifedipine-sensitive LVA Ca 2+ current. The voltage protocol is shown at the top. The membrane was depolarized to -50 mV from different holding potentials between -105 and -75 mV. The duration of the prepulse impulse was 500 ms. B , the inactivation curve fitted by a Boltzmann equation ( I/I max =[1 + exp( V - V 0.5 /k)] −1 , where I is the current amplitude, I max is the maximum current amplitude, V is the voltage, V 0.5 is the half-inactivation voltage and k is the slope factor) with V 0.5 = -86.9 mV and k = 3.4 mV ( n = 7).
    Figure Legend Snippet: Steady-state inactivation of LVA Ca 2+ current in P2 neurones A , voltage dependence of steady-state inactivation of the nifedipine-sensitive LVA Ca 2+ current. The voltage protocol is shown at the top. The membrane was depolarized to -50 mV from different holding potentials between -105 and -75 mV. The duration of the prepulse impulse was 500 ms. B , the inactivation curve fitted by a Boltzmann equation ( I/I max =[1 + exp( V - V 0.5 /k)] −1 , where I is the current amplitude, I max is the maximum current amplitude, V is the voltage, V 0.5 is the half-inactivation voltage and k is the slope factor) with V 0.5 = -86.9 mV and k = 3.4 mV ( n = 7).

    Techniques Used: Mass Spectrometry

    Blocking effect of nifedipine on LVA Ca 2+ current in P2 visual cortical neurones A , LVA Ca 2+ current recorded in P2 neurones before (Control) and after blocking by 100 μM nifedipine. The current was obtained by 35 mV step depolarization from a holding potential of -95 mV (top). B , the nifedipine-sensitive component was obtained by subtracting LVA Ca 2+ current after blocking by 100 μM nifedipine from the control LVA Ca 2+ current. It was fitted in terms of the m 2 h model (continuous line) with the inactivation time constant (τ h ) indicated.
    Figure Legend Snippet: Blocking effect of nifedipine on LVA Ca 2+ current in P2 visual cortical neurones A , LVA Ca 2+ current recorded in P2 neurones before (Control) and after blocking by 100 μM nifedipine. The current was obtained by 35 mV step depolarization from a holding potential of -95 mV (top). B , the nifedipine-sensitive component was obtained by subtracting LVA Ca 2+ current after blocking by 100 μM nifedipine from the control LVA Ca 2+ current. It was fitted in terms of the m 2 h model (continuous line) with the inactivation time constant (τ h ) indicated.

    Techniques Used: Blocking Assay

    12) Product Images from "Grass Carp Prolactin Gene: Structural Characterization and Signal Transduction for PACAP-induced Prolactin Promoter Activity"

    Article Title: Grass Carp Prolactin Gene: Structural Characterization and Signal Transduction for PACAP-induced Prolactin Promoter Activity

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-23092-0

    Ca 2+ -dependent of PACAP- and Forskolin-induced PRL promoter activity in αT3-1 Cells. αT3-1 cells were transiently transfected with pPRL(−1156).LUC for 6 h by using lipofectamine. After 18 h recovery, the cells were incubated with respective drugs. The cells were treated for 24 hr with increasing doses of ( A ) Ca 2+ ionophore A23187 or ( B ) L-type VSCC activator Bay K8644. Inhibiting extracellular Ca 2+ entry on PRL mRNA expression in carp pituitary cells was examined. In this study, αT3-1 cells over-expressed pPRL(−1156).LUC were treated with ( C ) oPACAP 38 (10 nM, 24 hrs) or ( D ) Forskolin (100 nM, 24 hrs) in the Ca 2+ -free medium (with different doses of EGTA). Further, αT3-1 cells over-expressed pPRL(−1156).LUC were treated with ( E ) oPACAP 38 (10 nM, 24 hrs) or ( F ) Forskolin (100 nM, 24 hrs) in the presence or absence of L-type VSCC blocker nifedipine (10 μM). After drug treatment, cell lysate was prepared for dual-luciferase measurement. Data presented were expressed as percentage of control by conversing the ratio of firefly and renilla luciferase in the same sample. Data presented are expressed as mean ± SEM (n = 4) and different letters denote a significant difference at p
    Figure Legend Snippet: Ca 2+ -dependent of PACAP- and Forskolin-induced PRL promoter activity in αT3-1 Cells. αT3-1 cells were transiently transfected with pPRL(−1156).LUC for 6 h by using lipofectamine. After 18 h recovery, the cells were incubated with respective drugs. The cells were treated for 24 hr with increasing doses of ( A ) Ca 2+ ionophore A23187 or ( B ) L-type VSCC activator Bay K8644. Inhibiting extracellular Ca 2+ entry on PRL mRNA expression in carp pituitary cells was examined. In this study, αT3-1 cells over-expressed pPRL(−1156).LUC were treated with ( C ) oPACAP 38 (10 nM, 24 hrs) or ( D ) Forskolin (100 nM, 24 hrs) in the Ca 2+ -free medium (with different doses of EGTA). Further, αT3-1 cells over-expressed pPRL(−1156).LUC were treated with ( E ) oPACAP 38 (10 nM, 24 hrs) or ( F ) Forskolin (100 nM, 24 hrs) in the presence or absence of L-type VSCC blocker nifedipine (10 μM). After drug treatment, cell lysate was prepared for dual-luciferase measurement. Data presented were expressed as percentage of control by conversing the ratio of firefly and renilla luciferase in the same sample. Data presented are expressed as mean ± SEM (n = 4) and different letters denote a significant difference at p

    Techniques Used: Activity Assay, Transfection, Incubation, Expressing, Luciferase

    13) Product Images from "PPAR-? Activation Increases Insulin Secretion through the Up-regulation of the Free Fatty Acid Receptor GPR40 in Pancreatic ?-Cells"

    Article Title: PPAR-? Activation Increases Insulin Secretion through the Up-regulation of the Free Fatty Acid Receptor GPR40 in Pancreatic ?-Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0050128

    RGZ induces intracellular calcium mobilization from extra- and intra-cellular sources. (A) Effects of nifedipine (10 mM), thapsigargin (0.1 µM), and GLUT2 sequence-specific silencing with RNAi on 10 µM RGZ-induced intracellular calcium mobilization and (B) insulin secretion (ANOVA within same glucose conditions: n = 4, * P
    Figure Legend Snippet: RGZ induces intracellular calcium mobilization from extra- and intra-cellular sources. (A) Effects of nifedipine (10 mM), thapsigargin (0.1 µM), and GLUT2 sequence-specific silencing with RNAi on 10 µM RGZ-induced intracellular calcium mobilization and (B) insulin secretion (ANOVA within same glucose conditions: n = 4, * P

    Techniques Used: Sequencing

    14) Product Images from "L-Type Calcium Channel Inhibition Contributes to the Proarrhythmic Effects of Aconitine in Human Cardiomyocytes"

    Article Title: L-Type Calcium Channel Inhibition Contributes to the Proarrhythmic Effects of Aconitine in Human Cardiomyocytes

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0168435

    Effects of ACO on I Ca,L in hiPSC-CMs. (A) Representative traces of the voltage-gated LTCC current I Ca,L recorded from a hiPSC-CM at baseline followed by exposure of 1 μM ACO and addition of 1 μM nifedipine. (B) Representative traces and I-V curves recorded from hiPSC-CMs exposed to 1 μM ACO followed by 1 μM Bay K-8644. * p
    Figure Legend Snippet: Effects of ACO on I Ca,L in hiPSC-CMs. (A) Representative traces of the voltage-gated LTCC current I Ca,L recorded from a hiPSC-CM at baseline followed by exposure of 1 μM ACO and addition of 1 μM nifedipine. (B) Representative traces and I-V curves recorded from hiPSC-CMs exposed to 1 μM ACO followed by 1 μM Bay K-8644. * p

    Techniques Used:

    Effects of ACO on action potentials of hiPSC-CMs. (A) Representative AP waveforms recorded in a hiPSC-CM with 120 seconds (s) exposure of ACO at 0.3 and 3.0 μM and 180s and 300s exposure of ACO at 3.0 μM. Increased beating frequencies and decreased APD and APA were observed with short-term (120s) ACO treatment. Prolonged treatment of ACO at 3.0 μM led to frequent DADs and rapid irregular VF-like AP changes. (B),Representative AP waveforms recorded in a hiPSC-CM exposed to 0.3 μM nifedipine for 60s ~ 240s. Increased beating frequencies and decreased APD occurred at 60s while DADs emerged at 180s. APs were suppressed at 240s. The arrows indicate DADs.
    Figure Legend Snippet: Effects of ACO on action potentials of hiPSC-CMs. (A) Representative AP waveforms recorded in a hiPSC-CM with 120 seconds (s) exposure of ACO at 0.3 and 3.0 μM and 180s and 300s exposure of ACO at 3.0 μM. Increased beating frequencies and decreased APD and APA were observed with short-term (120s) ACO treatment. Prolonged treatment of ACO at 3.0 μM led to frequent DADs and rapid irregular VF-like AP changes. (B),Representative AP waveforms recorded in a hiPSC-CM exposed to 0.3 μM nifedipine for 60s ~ 240s. Increased beating frequencies and decreased APD occurred at 60s while DADs emerged at 180s. APs were suppressed at 240s. The arrows indicate DADs.

    Techniques Used:

    15) Product Images from "Despite increased plasma concentration, inflammation reduces potency of calcium channel antagonists due to lower binding to the rat heart"

    Article Title: Despite increased plasma concentration, inflammation reduces potency of calcium channel antagonists due to lower binding to the rat heart

    Journal: British Journal of Pharmacology

    doi: 10.1038/sj.bjp.0705202

    Nifedipine plasma concentration–time profile in control and INF-induced inflamed rats following administration of single i.v. doses of 0.1 mg kg −1 ( n =8/group).
    Figure Legend Snippet: Nifedipine plasma concentration–time profile in control and INF-induced inflamed rats following administration of single i.v. doses of 0.1 mg kg −1 ( n =8/group).

    Techniques Used: Concentration Assay

    Effect on inflammation on the potency of verapamil (a) nifedipine (b) to influence PR interval prolongation (PR) and (HR). Columns present maximum percent change from baseline (MAX) or the area under the percent effect change from the baseline versus time curve (AUEC, % h −1 ) during the 0–8 h period postdose; * denoted a significant difference between control and inflamed group; n =8/group.
    Figure Legend Snippet: Effect on inflammation on the potency of verapamil (a) nifedipine (b) to influence PR interval prolongation (PR) and (HR). Columns present maximum percent change from baseline (MAX) or the area under the percent effect change from the baseline versus time curve (AUEC, % h −1 ) during the 0–8 h period postdose; * denoted a significant difference between control and inflamed group; n =8/group.

    Techniques Used:

    16) Product Images from "Evaluation of Antidiabetic Effects of the Traditional Medicinal Plant Gynostemma pentaphyllum and the Possible Mechanisms of Insulin Release"

    Article Title: Evaluation of Antidiabetic Effects of the Traditional Medicinal Plant Gynostemma pentaphyllum and the Possible Mechanisms of Insulin Release

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    doi: 10.1155/2015/120572

    Effect of Gynostemma pentaphyllum ( GP ) with or without nifedipine (N) on glucose stimulated insulin secretion from isolated GK rat islets. ∗∗∗ P
    Figure Legend Snippet: Effect of Gynostemma pentaphyllum ( GP ) with or without nifedipine (N) on glucose stimulated insulin secretion from isolated GK rat islets. ∗∗∗ P

    Techniques Used: Isolation

    17) Product Images from "Relaxant and anti-inflammatory effect of two thalidomide analogs as PDE-4 inhibitors in pregnant rat uterus"

    Article Title: Relaxant and anti-inflammatory effect of two thalidomide analogs as PDE-4 inhibitors in pregnant rat uterus

    Journal: The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology

    doi: 10.4196/kjpp.2017.21.4.429

    Inhibitory effect of thalidomide analogs, rolipram, forskolin and nifedipine on PGF2α-induced phasic contractions. (a) Concentration-response curves of uterine strips of pregnant rat. Each point in both graphs indicates the mean of 6 experiments (n=6) for thalidomide analogs, rolipram, forskolin and nifedipine; the vertical bars represents the standard error of the mean (SEM). (b) Typical recording of PGF2α-stimulated phasic contractions inhibited by thalidomide analogs in concentration-dependent manner. * Different from rolipram, p
    Figure Legend Snippet: Inhibitory effect of thalidomide analogs, rolipram, forskolin and nifedipine on PGF2α-induced phasic contractions. (a) Concentration-response curves of uterine strips of pregnant rat. Each point in both graphs indicates the mean of 6 experiments (n=6) for thalidomide analogs, rolipram, forskolin and nifedipine; the vertical bars represents the standard error of the mean (SEM). (b) Typical recording of PGF2α-stimulated phasic contractions inhibited by thalidomide analogs in concentration-dependent manner. * Different from rolipram, p

    Techniques Used: Concentration Assay

    Inhibitory effect of thalidomide analogs, rolipram, forskolin and nifedipine on KCl-induced phasic contractions. (a) Concentration-response curves of uterine strips of pregnant rat. Each point in both graphs indicates the mean of 6 experiments (n=6) for thalidomide analogs, rolipram, forskolin and nifedipine; the vertical bars represents the standard error of the mean (SEM). (b) Typical recording of KCl-stimulated phasic contractions inhibited by thalidomide analogs in concentration-dependent manner. * Different from rolipram, p
    Figure Legend Snippet: Inhibitory effect of thalidomide analogs, rolipram, forskolin and nifedipine on KCl-induced phasic contractions. (a) Concentration-response curves of uterine strips of pregnant rat. Each point in both graphs indicates the mean of 6 experiments (n=6) for thalidomide analogs, rolipram, forskolin and nifedipine; the vertical bars represents the standard error of the mean (SEM). (b) Typical recording of KCl-stimulated phasic contractions inhibited by thalidomide analogs in concentration-dependent manner. * Different from rolipram, p

    Techniques Used: Concentration Assay

    Inhibitory effect of thalidomide analogs, rolipram, forskolin and nifedipine on Ca 2+ -induced tonic contractions. (a) Concentration-response curves of uterine strips of pregnant rat. Each point in both graphs indicates the mean of 6 experiments (n=6) for thalidomide analogs, rolipram, forskolin and nifedipine; the vertical bars represents the standard error of the mean (SEM). (b) Typical recording of Ca 2+ -stimulated tonic contractions inhibited by thalidomide analogs, rolipram, forskolin and nifedipine in concentration-dependent form, * p
    Figure Legend Snippet: Inhibitory effect of thalidomide analogs, rolipram, forskolin and nifedipine on Ca 2+ -induced tonic contractions. (a) Concentration-response curves of uterine strips of pregnant rat. Each point in both graphs indicates the mean of 6 experiments (n=6) for thalidomide analogs, rolipram, forskolin and nifedipine; the vertical bars represents the standard error of the mean (SEM). (b) Typical recording of Ca 2+ -stimulated tonic contractions inhibited by thalidomide analogs, rolipram, forskolin and nifedipine in concentration-dependent form, * p

    Techniques Used: Concentration Assay

    18) Product Images from "Friedreich's ataxia induced pluripotent stem cell-derived cardiomyocytes display electrophysiological abnormalities and calcium handling deficiency"

    Article Title: Friedreich's ataxia induced pluripotent stem cell-derived cardiomyocytes display electrophysiological abnormalities and calcium handling deficiency

    Journal: Aging (Albany NY)

    doi: 10.18632/aging.101247

    Assessment of phenotypes in FRDA iPSC-derived cardiomyocytes (A) Beating rates (beats per minute, BPM), (B) corrected extracellular field potential durations (cFPD) and (C, D) the root of the mean of the sum of the square of the difference in the RR interval (RMSSD) (ms). Data shows RMSSD at basal ( C ) and 10 −6 M ( D ) isoprenaline ± nifedipine (NIF). (E) Representative Ca 2+ transients. (F) Diastolic, (G) systolic and (H) amplitude Ca 2+ in Control and FRDA- cardiomyocytes. ( A-D ) Data are mean ± SEM of combined values of 3 clones of each line (n=3 per line) and as a pool of all 3 clones of all FRDA lines (n=9 FRDA independent samples) and control cardiomyocytes (n=6). ( F-H ) Data are mean ± SEM of combined values of control cardiomyocytes (n=5), all 3 clones of each FRDA line (n=8-14 per line) and as a pool of all 3 clones of all FRDA lines (n=35 FRDA independent samples). Statistics: ( A-D, F-H ) One-way ANOVA followed by Bonferroni's multiple comparison test, * p
    Figure Legend Snippet: Assessment of phenotypes in FRDA iPSC-derived cardiomyocytes (A) Beating rates (beats per minute, BPM), (B) corrected extracellular field potential durations (cFPD) and (C, D) the root of the mean of the sum of the square of the difference in the RR interval (RMSSD) (ms). Data shows RMSSD at basal ( C ) and 10 −6 M ( D ) isoprenaline ± nifedipine (NIF). (E) Representative Ca 2+ transients. (F) Diastolic, (G) systolic and (H) amplitude Ca 2+ in Control and FRDA- cardiomyocytes. ( A-D ) Data are mean ± SEM of combined values of 3 clones of each line (n=3 per line) and as a pool of all 3 clones of all FRDA lines (n=9 FRDA independent samples) and control cardiomyocytes (n=6). ( F-H ) Data are mean ± SEM of combined values of control cardiomyocytes (n=5), all 3 clones of each FRDA line (n=8-14 per line) and as a pool of all 3 clones of all FRDA lines (n=35 FRDA independent samples). Statistics: ( A-D, F-H ) One-way ANOVA followed by Bonferroni's multiple comparison test, * p

    Techniques Used: Derivative Assay, Mass Spectrometry, Clone Assay

    19) Product Images from "Sialoglycosylation of RBC in Visceral Leishmaniasis Leads to Enhanced Oxidative Stress, Calpain-Induced Fragmentation of Spectrin and Hemolysis"

    Article Title: Sialoglycosylation of RBC in Visceral Leishmaniasis Leads to Enhanced Oxidative Stress, Calpain-Induced Fragmentation of Spectrin and Hemolysis

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0042361

    Calcium influx into RBC upon sensitization with anti-9- O -AcSGP IgG VL antibodies. For all experiments, erythrocytes were washed and loaded with the Ca 2+ -indicator fluorochrome Fluo-3/AM in Ringer solution. A23187-treated Fluo-3/AM-loaded RBC VL served as positive controls (black line) and A23187-treated cells in the presence of EGTA as negative controls (gray background). A. Fluo-3/AM loaded RBC VL and RBC N (2×10 7 ) were left unsensitized or sensitized with varying concentrations of anti-9- O -AcSGP IgG VL or anti-9- O -AcSGP IgG NHS , respectively, (0–40 µg/ml) in Ringer solution for 30 min at 37°C. After washing the cells twice with same solution the fluorescence intensities of the Ca 2+ -Fluo-3 complexes was determined by spectrofluorimetry and the levels of intracellular calcium calculated as described in Materials and Methods . B. Cells treated as in A with 0.5 µg/ml (red line), 1.0 µg/ml (green line) and 2.5 µg/ml (pink line) anti-9- O -AcSGP IgG VL were analyzed by flow cytometry to determine the fraction of responding RBC. C. Similarly, RBC N were analyzed without and with sensitization with 5 µg/ml anti-9-O-AcSGP IgG NHS (blue line). D–E. Time dependent increase of intracellular Ca 2+ in RBC VL after sensitization with anti-9- O -AcSGP IgG VL (2.5 µg/ml) for 5 min (red line), 10 min (green line), 20 min (pink line) and 30 min (blue line) at 37°C. Cells were washed and analyzed by flow cytometry. D. Histogram representation; E. Mean fluorescence intensities calculated from D. F–G. Inhibition of the Ca 2+ influx into RBC sensitized with anti-9- O -AcSGP IgG VL . Prior to sensitization with anti-9- O -AcSGP-IgG VL (2.5 µg/ml), the cells were incubated without (green line) or with the P/Q-type channel blocker ω-agatoxin TK (1 µM, pink line, F ), or without (green line) or with the L-type channel blocker nifedipine (10 µM, blue line, G ) and analyzed by flow cytometry.
    Figure Legend Snippet: Calcium influx into RBC upon sensitization with anti-9- O -AcSGP IgG VL antibodies. For all experiments, erythrocytes were washed and loaded with the Ca 2+ -indicator fluorochrome Fluo-3/AM in Ringer solution. A23187-treated Fluo-3/AM-loaded RBC VL served as positive controls (black line) and A23187-treated cells in the presence of EGTA as negative controls (gray background). A. Fluo-3/AM loaded RBC VL and RBC N (2×10 7 ) were left unsensitized or sensitized with varying concentrations of anti-9- O -AcSGP IgG VL or anti-9- O -AcSGP IgG NHS , respectively, (0–40 µg/ml) in Ringer solution for 30 min at 37°C. After washing the cells twice with same solution the fluorescence intensities of the Ca 2+ -Fluo-3 complexes was determined by spectrofluorimetry and the levels of intracellular calcium calculated as described in Materials and Methods . B. Cells treated as in A with 0.5 µg/ml (red line), 1.0 µg/ml (green line) and 2.5 µg/ml (pink line) anti-9- O -AcSGP IgG VL were analyzed by flow cytometry to determine the fraction of responding RBC. C. Similarly, RBC N were analyzed without and with sensitization with 5 µg/ml anti-9-O-AcSGP IgG NHS (blue line). D–E. Time dependent increase of intracellular Ca 2+ in RBC VL after sensitization with anti-9- O -AcSGP IgG VL (2.5 µg/ml) for 5 min (red line), 10 min (green line), 20 min (pink line) and 30 min (blue line) at 37°C. Cells were washed and analyzed by flow cytometry. D. Histogram representation; E. Mean fluorescence intensities calculated from D. F–G. Inhibition of the Ca 2+ influx into RBC sensitized with anti-9- O -AcSGP IgG VL . Prior to sensitization with anti-9- O -AcSGP-IgG VL (2.5 µg/ml), the cells were incubated without (green line) or with the P/Q-type channel blocker ω-agatoxin TK (1 µM, pink line, F ), or without (green line) or with the L-type channel blocker nifedipine (10 µM, blue line, G ) and analyzed by flow cytometry.

    Techniques Used: Fluorescence, Flow Cytometry, Cytometry, Inhibition, Incubation

    20) Product Images from "Defining the ionic mechanisms of optogenetic control of vascular tone by channelrhodopsin‐2) Defining the ionic mechanisms of optogenetic control of vascular tone by channelrhodopsin‐2"

    Article Title: Defining the ionic mechanisms of optogenetic control of vascular tone by channelrhodopsin‐2) Defining the ionic mechanisms of optogenetic control of vascular tone by channelrhodopsin‐2

    Journal: British Journal of Pharmacology

    doi: 10.1111/bph.14183

    Effect of pharmacological ion channel modulation and ionic substitution on blue light‐induced tension of aortic rings obtained from ChR2(H134R)‐SM mice. (A) Top panels represent isometric tension recordings obtained from aortic rings isolated from ChR2(H134R)‐SM mice in response to 0.23 mW·mm −2 blue light in the presence of PSS (control) or a nominally Ca 2+ ‐free PSS (0 Ca 2+ ). The lower panel represents mean tension versus blue light intensity relationship for experiments conducted in Ca 2+ ‐free PSS ( N = 5, n = 10). The sigmoidal curve (dashed) is the Hill fit (Equation (5) ) of the aortic ring tension versus blue light intensity relationship presented in Figure 2 B. (B) Top panel represents isometric tension recordings obtained from an aortic ring isolated from ChR2(H134R)‐SM mice in response to 0.23 mW·mm −2 blue light in the presence of PSS supplemented with nifedipine (1 μM). The lower panel represents mean tension versus blue light intensity relationship for experiments conducted in PSS supplemented with nifedipine (1 μM) ( N = 7, n = 8). Continuous sigmoidal curve through squares symbols indicates the best fit of the data with Equation (5) . Dashed sigmoidal curve is the Hill fit (Equation (5) ) of the aortic ring tension versus blue light intensity relationship presented in Figure 2 B. (C) Mean tension in response to blue light stimulations in PSS supplemented with 3 μM ryanodine ( N = 6, n = 8) or 60 μM 2‐APB ( N = 6, n = 8), as indicated. Open circles refer to experiments conducted in control PSS solution and are replotted from Figure 2 B. (D) Mean tension in response to blue light stimulations in PSS supplemented with either MONNA (3 μM) ( N = 5, n = 10) or Ani9 (1 μM) ( N = 5, n = 10). Open circles refer to experiments conducted in control PSS solution and are replotted from Figure 2 B. (E) Mean tension in response to blue light stimulations in PSS supplemented with either clotrimazole (10 μM) ( N = 5, n = 9) or 9‐phenanthrol (50 μM) ( N = 5, n = 5). Open circles refer to experiments conducted in control PSS solution and are replotted from Figure 2 B. * P
    Figure Legend Snippet: Effect of pharmacological ion channel modulation and ionic substitution on blue light‐induced tension of aortic rings obtained from ChR2(H134R)‐SM mice. (A) Top panels represent isometric tension recordings obtained from aortic rings isolated from ChR2(H134R)‐SM mice in response to 0.23 mW·mm −2 blue light in the presence of PSS (control) or a nominally Ca 2+ ‐free PSS (0 Ca 2+ ). The lower panel represents mean tension versus blue light intensity relationship for experiments conducted in Ca 2+ ‐free PSS ( N = 5, n = 10). The sigmoidal curve (dashed) is the Hill fit (Equation (5) ) of the aortic ring tension versus blue light intensity relationship presented in Figure 2 B. (B) Top panel represents isometric tension recordings obtained from an aortic ring isolated from ChR2(H134R)‐SM mice in response to 0.23 mW·mm −2 blue light in the presence of PSS supplemented with nifedipine (1 μM). The lower panel represents mean tension versus blue light intensity relationship for experiments conducted in PSS supplemented with nifedipine (1 μM) ( N = 7, n = 8). Continuous sigmoidal curve through squares symbols indicates the best fit of the data with Equation (5) . Dashed sigmoidal curve is the Hill fit (Equation (5) ) of the aortic ring tension versus blue light intensity relationship presented in Figure 2 B. (C) Mean tension in response to blue light stimulations in PSS supplemented with 3 μM ryanodine ( N = 6, n = 8) or 60 μM 2‐APB ( N = 6, n = 8), as indicated. Open circles refer to experiments conducted in control PSS solution and are replotted from Figure 2 B. (D) Mean tension in response to blue light stimulations in PSS supplemented with either MONNA (3 μM) ( N = 5, n = 10) or Ani9 (1 μM) ( N = 5, n = 10). Open circles refer to experiments conducted in control PSS solution and are replotted from Figure 2 B. (E) Mean tension in response to blue light stimulations in PSS supplemented with either clotrimazole (10 μM) ( N = 5, n = 9) or 9‐phenanthrol (50 μM) ( N = 5, n = 5). Open circles refer to experiments conducted in control PSS solution and are replotted from Figure 2 B. * P

    Techniques Used: Mouse Assay, Isolation

    21) Product Images from "Dissecting out the Complex Ca2+-Mediated Phenylephrine-Induced Contractions of Mouse Aortic Segments"

    Article Title: Dissecting out the Complex Ca2+-Mediated Phenylephrine-Induced Contractions of Mouse Aortic Segments

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0121634

    Effects of VGCC blockers on isometric contractions by PE. Nifedipine, verapamil and diltiazem partly inhibit isometric contractions induced by 1 μM PE in organ bath-mounted aortic segments. A) Contractions induced by 1 μM PE after incubating the segments with 1 to 100 nM nifedipine (n = 4); B) Ca 2+ channel blocker (CCB) concentration-response curves for the inhibition of contractions induced by 1 μM PE.
    Figure Legend Snippet: Effects of VGCC blockers on isometric contractions by PE. Nifedipine, verapamil and diltiazem partly inhibit isometric contractions induced by 1 μM PE in organ bath-mounted aortic segments. A) Contractions induced by 1 μM PE after incubating the segments with 1 to 100 nM nifedipine (n = 4); B) Ca 2+ channel blocker (CCB) concentration-response curves for the inhibition of contractions induced by 1 μM PE.

    Techniques Used: Concentration Assay, Inhibition

    22) Product Images from "L-type calcium channels and MAP kinase contribute to thyrotropin-releasing hormone-induced depolarization in thalamic paraventricular nucleus neurons"

    Article Title: L-type calcium channels and MAP kinase contribute to thyrotropin-releasing hormone-induced depolarization in thalamic paraventricular nucleus neurons

    Journal: American Journal of Physiology - Regulatory, Integrative and Comparative Physiology

    doi: 10.1152/ajpregu.00082.2016

    Activation of L-type Ca 2+ channels is essential for the coupling of TRH receptor to both G protein-coupled inwardly rectifying K (GIRK)- and transient receptor potential canonical (TRPC)-like channels. Sample voltage-clamp traces done in the presence of 1 μM tetrodotoxin (TTX). A: typical trace showing reduced response to bath-applied TRH (100 nM for 60 s) in ACSF with nominally 0 mM Ca 2+ (for 15 min). B: trace from another PVT neuron illustrates normal response to TRH in the presence of T-type Ca 2+ channel blocker Z941 (1 μM for 10 min). C: trace from another PVT neuron to illustrate a reduced TRH-induced inward current in the presence of L-type Ca 2+ channel blocker nifedipine (3 μM for 10 min). D: trace exhibiting both enhanced amplitude and duration of TRH-induced inward current during coadministration of L-type Ca 2+ channel agonist BayK8644 (10 μM). E: summary histogram (number reflects cells tested in each condition) illustrates TRH-induced inward current either alone (100 nM; black bars) and when applied in ACSF with nominally 0 mM Ca 2+ , Z941 (1 μM), cadmium (100 μM for 10 min), ω-conotoxin GVIA (400 nM) and ω-Agatoxin IVA (con/aga; 200 nM), nifedipine (3 μM), and BayK8644 (10 μM). Note that TRH (black bars) or TRH in the presence of either nifedipine (dark gray bars) or BayK8644 (dark gray patterned bars) was applied in three different external media: control ACSF (expressing GIRK+TRPC currents), ACSF where NaCl was replaced with Tris-Cl to isolate GIRK-like channels (low Na + -GIRK), and ACSF with 1.3 mM Ba 2+ to isolate TRPC-like channels (1.3 mM Ba 2+ -TRPC). Data are expressed as means ± SE. * P
    Figure Legend Snippet: Activation of L-type Ca 2+ channels is essential for the coupling of TRH receptor to both G protein-coupled inwardly rectifying K (GIRK)- and transient receptor potential canonical (TRPC)-like channels. Sample voltage-clamp traces done in the presence of 1 μM tetrodotoxin (TTX). A: typical trace showing reduced response to bath-applied TRH (100 nM for 60 s) in ACSF with nominally 0 mM Ca 2+ (for 15 min). B: trace from another PVT neuron illustrates normal response to TRH in the presence of T-type Ca 2+ channel blocker Z941 (1 μM for 10 min). C: trace from another PVT neuron to illustrate a reduced TRH-induced inward current in the presence of L-type Ca 2+ channel blocker nifedipine (3 μM for 10 min). D: trace exhibiting both enhanced amplitude and duration of TRH-induced inward current during coadministration of L-type Ca 2+ channel agonist BayK8644 (10 μM). E: summary histogram (number reflects cells tested in each condition) illustrates TRH-induced inward current either alone (100 nM; black bars) and when applied in ACSF with nominally 0 mM Ca 2+ , Z941 (1 μM), cadmium (100 μM for 10 min), ω-conotoxin GVIA (400 nM) and ω-Agatoxin IVA (con/aga; 200 nM), nifedipine (3 μM), and BayK8644 (10 μM). Note that TRH (black bars) or TRH in the presence of either nifedipine (dark gray bars) or BayK8644 (dark gray patterned bars) was applied in three different external media: control ACSF (expressing GIRK+TRPC currents), ACSF where NaCl was replaced with Tris-Cl to isolate GIRK-like channels (low Na + -GIRK), and ACSF with 1.3 mM Ba 2+ to isolate TRPC-like channels (1.3 mM Ba 2+ -TRPC). Data are expressed as means ± SE. * P

    Techniques Used: Activation Assay, Expressing

    23) Product Images from "L-type Ca2+ channel blockers promote Ca2+ accumulation when dopamine receptors are activated in striatal neurons"

    Article Title: L-type Ca2+ channel blockers promote Ca2+ accumulation when dopamine receptors are activated in striatal neurons

    Journal: Brain research. Molecular brain research

    doi: 10.1016/j.molbrainres.2004.08.007

    Glutamate- and NMDA-mediated CREB phosphorylation is inhibited by nifedipine. (A) Immunoblot showing that CREB phosphorylation by glutamate (50 µM) is blocked by nifedipine (20 µM). (B) Average fold induction of p -CREB/CREB, ±S.E.M., of n =6 samples in three independent experiments; untreated control levels were arbitrarily set to “1”. (C) Immunoblot showing that CREB phosphorylation by NMDA (50 µM) is blocked by nifedipine (20 µM). (D) Average fold induction of p -CREB/CREB, ±S.E.M., of n =4 samples in two independent experiments; untreated control levels were arbitrarily set to “1”. (E, F) Immunoblot showing the inhibitory potential of 10 and 20 µM nifedipine on FPL 64176-mediated CREB phosphorylation (E) and on NMDA-mediated CREB phosphorylation (F). Similar results were obtained with glutamate and verapamil (not shown). ** p
    Figure Legend Snippet: Glutamate- and NMDA-mediated CREB phosphorylation is inhibited by nifedipine. (A) Immunoblot showing that CREB phosphorylation by glutamate (50 µM) is blocked by nifedipine (20 µM). (B) Average fold induction of p -CREB/CREB, ±S.E.M., of n =6 samples in three independent experiments; untreated control levels were arbitrarily set to “1”. (C) Immunoblot showing that CREB phosphorylation by NMDA (50 µM) is blocked by nifedipine (20 µM). (D) Average fold induction of p -CREB/CREB, ±S.E.M., of n =4 samples in two independent experiments; untreated control levels were arbitrarily set to “1”. (E, F) Immunoblot showing the inhibitory potential of 10 and 20 µM nifedipine on FPL 64176-mediated CREB phosphorylation (E) and on NMDA-mediated CREB phosphorylation (F). Similar results were obtained with glutamate and verapamil (not shown). ** p

    Techniques Used:

    In the presence of L-type Ca 2+ channel blockers, DA mediates CREB phosphorylation independently of NMDA receptors. (A) Immunoblot showing that the inhibition of DA-mediated CREB phosphorylation by MK 801 is reversed by nifedipine. (B) Average fold induction of p -CREB, ±S.E.M., of n =6 samples in three independent gels; untreated control levels were arbitrarily set to “1”. *** p
    Figure Legend Snippet: In the presence of L-type Ca 2+ channel blockers, DA mediates CREB phosphorylation independently of NMDA receptors. (A) Immunoblot showing that the inhibition of DA-mediated CREB phosphorylation by MK 801 is reversed by nifedipine. (B) Average fold induction of p -CREB, ±S.E.M., of n =6 samples in three independent gels; untreated control levels were arbitrarily set to “1”. *** p

    Techniques Used: Inhibition

    24) Product Images from "Inhibitory control of plateau properties in dorsal horn neurones in the turtle spinal cord in vitro"

    Article Title: Inhibitory control of plateau properties in dorsal horn neurones in the turtle spinal cord in vitro

    Journal: The Journal of Physiology

    doi: 10.1111/j.1469-7793.1998.795bv.x

    Baclofen inhibited the plateau potential A , in the presence of TTX (1 μM) replacement of Ca 2+ with Ba 2+ and the blockade of K + conductances with TEA (15 mM) and apamin (0.5 μM) resulted in a high-amplitude, long-lasting plateau ( a , control). Under these conditions baclofen (50 μM) reduced significantly the duration of the plateau potential ( a , baclofen). The response to the 3rd, 5th, 7th and 8th responses after baclofen illustrate the progressive decrease in the duration of the plateau. The baclofen-induced inhibition of the plateau potential reversed upon washout of the drug ( b , wash). B , in another cell, the plateau potential recorded under the same conditions as in A was reduced by baclofen (25 μM). The response recovered after washout of baclofen ( b ) and was subsequently inhibited by nifedipine (10 μM). Further addition of baclofen (25 μM) did not significantly affect the plateau potential ( b ).
    Figure Legend Snippet: Baclofen inhibited the plateau potential A , in the presence of TTX (1 μM) replacement of Ca 2+ with Ba 2+ and the blockade of K + conductances with TEA (15 mM) and apamin (0.5 μM) resulted in a high-amplitude, long-lasting plateau ( a , control). Under these conditions baclofen (50 μM) reduced significantly the duration of the plateau potential ( a , baclofen). The response to the 3rd, 5th, 7th and 8th responses after baclofen illustrate the progressive decrease in the duration of the plateau. The baclofen-induced inhibition of the plateau potential reversed upon washout of the drug ( b , wash). B , in another cell, the plateau potential recorded under the same conditions as in A was reduced by baclofen (25 μM). The response recovered after washout of baclofen ( b ) and was subsequently inhibited by nifedipine (10 μM). Further addition of baclofen (25 μM) did not significantly affect the plateau potential ( b ).

    Techniques Used: Inhibition

    Blockade of inhibition promoted prolonged after-discharges and wind-up A , in normal medium, a single shock to the DR (40 μA) produced a brief burst of APs followed by polysynaptic IPSPs ( a , upper trace). After addition of strychnine (20 μM), the initial burst increased and was followed by a sustained firing ( a , lower trace). The time course of the overall response is shown in b . The duration of the response decreased when the cell was hyperpolarized from -55 mV ( b , upper trace) to -105 mV ( b , lower trace). B , repetitive stimulation of DR (30 μA at 0.3 Hz) in control medium elicited a weak wind-up of the synaptic response ( a ). A clear wind-up of the response to DR stimulation (12 μA) was seen after blockade of glycinergic receptors with strychnine (20 μM) ( b ). AP-5 (100 μM) decreased the response to DR stimulation but did not block wind-up ( c ). Addition of nifedipine (10 μM) completely blocked wind-up ( d ). All data are from the same cell.
    Figure Legend Snippet: Blockade of inhibition promoted prolonged after-discharges and wind-up A , in normal medium, a single shock to the DR (40 μA) produced a brief burst of APs followed by polysynaptic IPSPs ( a , upper trace). After addition of strychnine (20 μM), the initial burst increased and was followed by a sustained firing ( a , lower trace). The time course of the overall response is shown in b . The duration of the response decreased when the cell was hyperpolarized from -55 mV ( b , upper trace) to -105 mV ( b , lower trace). B , repetitive stimulation of DR (30 μA at 0.3 Hz) in control medium elicited a weak wind-up of the synaptic response ( a ). A clear wind-up of the response to DR stimulation (12 μA) was seen after blockade of glycinergic receptors with strychnine (20 μM) ( b ). AP-5 (100 μM) decreased the response to DR stimulation but did not block wind-up ( c ). Addition of nifedipine (10 μM) completely blocked wind-up ( d ). All data are from the same cell.

    Techniques Used: Inhibition, Produced, Blocking Assay

    25) Product Images from "Mechanosensory S-neurons rather than AH-neurons appear to generate a rhythmic motor pattern in guinea-pig distal colon"

    Article Title: Mechanosensory S-neurons rather than AH-neurons appear to generate a rhythmic motor pattern in guinea-pig distal colon

    Journal: The Journal of Physiology

    doi: 10.1113/jphysiol.2004.063586

    Properties of myenteric S-neurons in stretched preparations of distal colon while in the presence of nifedipine A , a tonic S-neuron firing in response to depolarizing current. Ai , while in the presence of a low Ca 2+ –high Mg 2+ solution, the neuron shown in A responded with a burst of action potentials in response to a ganglionic compression stimulus to the CM. B , in a different animal, an intrinsically active S-neuron showed an ongoing discharge of membrane noise represented by the unstable membrane potential. C , effects of membrane hyperpolarization on an S-neuron that had spontaneous action potentials and fast EPSPs. When the membrane potential was artificially hyperpolarized, the action potentials ceased, and only fast EPSPs were recorded. Fast EPSPs were detected because they increased in amplitude and had irregular amplitudes. Compare panels b, c and d, shown on an expanded scale in D – F . Recordings shown in A – C are all from different animals.
    Figure Legend Snippet: Properties of myenteric S-neurons in stretched preparations of distal colon while in the presence of nifedipine A , a tonic S-neuron firing in response to depolarizing current. Ai , while in the presence of a low Ca 2+ –high Mg 2+ solution, the neuron shown in A responded with a burst of action potentials in response to a ganglionic compression stimulus to the CM. B , in a different animal, an intrinsically active S-neuron showed an ongoing discharge of membrane noise represented by the unstable membrane potential. C , effects of membrane hyperpolarization on an S-neuron that had spontaneous action potentials and fast EPSPs. When the membrane potential was artificially hyperpolarized, the action potentials ceased, and only fast EPSPs were recorded. Fast EPSPs were detected because they increased in amplitude and had irregular amplitudes. Compare panels b, c and d, shown on an expanded scale in D – F . Recordings shown in A – C are all from different animals.

    Techniques Used:

    Electrical and morphological characteristics of a mechanosensory descending interneuron A , morphology of a pseudounipolar descending neuron that gave rise to two axons (more oral arrow). The thin axon appeared to provide synaptic outputs in the second row of ganglia (more anal arrow). The thicker darker axon appeared to leave a ganglia and enter the neighbouring CM (see *). B shows the cell body of this neuron with filamentous dendritic processes, one of which runs parallel to the CM fibres. C , this neuron had two bifurcating axons close to the axon hillock; see arrow. D , spontaneous proximal process potentials and action potentials occurred in this neuron under stretch and in the presence of nifedipine. When the membrane was artificially hyperpolarized by ∼50 mV the amplitude and interval between process potentials did not change, suggesting that these events were electrotonically invading the soma from a site distant to the cell body. E shows removal of hyperpolarizing holding current, where process potentials do not change characteristics. F , when simultaneous recordings were made from a CM cell and an S-neuron, single pulse transmural stimulation evoked FEPSPs (see arrow) and a single action potential, followed by a fast IJP in the CM. G , in addition to proximal process potentials, this neuron showed ongoing spontaneous fast EPSPs. These were identified because their amplitudes were highly variable. H , this neuron fired action potentials tonically in response to depolarizing current injection. The resting membrane potential of this neuron was −48 mV.
    Figure Legend Snippet: Electrical and morphological characteristics of a mechanosensory descending interneuron A , morphology of a pseudounipolar descending neuron that gave rise to two axons (more oral arrow). The thin axon appeared to provide synaptic outputs in the second row of ganglia (more anal arrow). The thicker darker axon appeared to leave a ganglia and enter the neighbouring CM (see *). B shows the cell body of this neuron with filamentous dendritic processes, one of which runs parallel to the CM fibres. C , this neuron had two bifurcating axons close to the axon hillock; see arrow. D , spontaneous proximal process potentials and action potentials occurred in this neuron under stretch and in the presence of nifedipine. When the membrane was artificially hyperpolarized by ∼50 mV the amplitude and interval between process potentials did not change, suggesting that these events were electrotonically invading the soma from a site distant to the cell body. E shows removal of hyperpolarizing holding current, where process potentials do not change characteristics. F , when simultaneous recordings were made from a CM cell and an S-neuron, single pulse transmural stimulation evoked FEPSPs (see arrow) and a single action potential, followed by a fast IJP in the CM. G , in addition to proximal process potentials, this neuron showed ongoing spontaneous fast EPSPs. These were identified because their amplitudes were highly variable. H , this neuron fired action potentials tonically in response to depolarizing current injection. The resting membrane potential of this neuron was −48 mV.

    Techniques Used: Injection

    Intrinsically active ascending interneuron in a stretched segment of distal colon A , ongoing action potentials and membrane noise recorded from a stretched preparation, while in the presence of nifedipine. Note the membrane noise during the interspike intervals. B , ongoing action potentials and noise are abolished by membrane hyperpolarization. This suggests that the action potentials arise close to or within the cell soma. C , morphology of this ascending interneuron, showing fine varicose synaptic outputs in the first and second rows of ganglia (see boxes 1 and 2, shown on enlarged scale in E and F ). This neuron had a long circumferentially projecting dendrite that arose from the soma. D , enlarged image of the neuronal soma and processes. E and F show the synaptic outputs of this ascending interneuron, expanded from boxes 1 and 2 in C . G and H show a short process that appears to enter the CM layer. G , when the soma is in focus, the end of this process is out of focus, suggesting it is not in the plane of the soma. H shows this process in focus (see arrow) and entering the CM layer, while the soma is now out of focus compared with G . The long axon of this neuron eventually left a ganglion (most oral ganglion shown in the top panel in C ) and entered and dived down through the CM ending in an expansion bulb on the submucosal surface of the CM (not shown), suggesting that it may terminate in the submucous plexus or the mucosa. Calibration bars represent 100 μm in C , 35 μm in D , 13 μm in E and F , and 17 μm in G and H .
    Figure Legend Snippet: Intrinsically active ascending interneuron in a stretched segment of distal colon A , ongoing action potentials and membrane noise recorded from a stretched preparation, while in the presence of nifedipine. Note the membrane noise during the interspike intervals. B , ongoing action potentials and noise are abolished by membrane hyperpolarization. This suggests that the action potentials arise close to or within the cell soma. C , morphology of this ascending interneuron, showing fine varicose synaptic outputs in the first and second rows of ganglia (see boxes 1 and 2, shown on enlarged scale in E and F ). This neuron had a long circumferentially projecting dendrite that arose from the soma. D , enlarged image of the neuronal soma and processes. E and F show the synaptic outputs of this ascending interneuron, expanded from boxes 1 and 2 in C . G and H show a short process that appears to enter the CM layer. G , when the soma is in focus, the end of this process is out of focus, suggesting it is not in the plane of the soma. H shows this process in focus (see arrow) and entering the CM layer, while the soma is now out of focus compared with G . The long axon of this neuron eventually left a ganglion (most oral ganglion shown in the top panel in C ) and entered and dived down through the CM ending in an expansion bulb on the submucosal surface of the CM (not shown), suggesting that it may terminate in the submucous plexus or the mucosa. Calibration bars represent 100 μm in C , 35 μm in D , 13 μm in E and F , and 17 μm in G and H .

    Techniques Used:

    Electrical activity recorded from a mechanosensory S-neuron in the myenteric plexus, when pinned under maintained circumferential stretch A , spontaneous action potentials and proximal process potentials occurred in this neuron when recorded in the presence of nifedipine, and were unaffected by the application of a low Ca 2+ –high Mg 2+ solution to block all synaptic transmission (see hatched bar). B shows an expanded portion of the recording in the low Ca 2+ –high Mg 2+ solution. Note, the similarity in amplitude of process potentials recorded in the low Ca 2+ solution. Some process potentials were sufficient to trigger a full somatic action potential. C , some spontaneous FEPSPs were recorded in this S-neuron prior to the application of the low Ca 2+ –high Mg 2+ solution. These are identified by their irregular amplitudes (see arrow). D , this neuron fired tonically in response to depolarizing current. E , in the presence of the low Ca 2+ –high Mg 2+ solution, removal of hyperpolarizing holding current increased the discharge of process potentials, suggesting that some mechanosensory ion channels may exist close to, or even in the cell soma itself. F , this neuron was an orally projecting uniaxonal filamentous neuron. The calibration bar represents 20 μm. The resting potential of this neuron was −53 mV.
    Figure Legend Snippet: Electrical activity recorded from a mechanosensory S-neuron in the myenteric plexus, when pinned under maintained circumferential stretch A , spontaneous action potentials and proximal process potentials occurred in this neuron when recorded in the presence of nifedipine, and were unaffected by the application of a low Ca 2+ –high Mg 2+ solution to block all synaptic transmission (see hatched bar). B shows an expanded portion of the recording in the low Ca 2+ –high Mg 2+ solution. Note, the similarity in amplitude of process potentials recorded in the low Ca 2+ solution. Some process potentials were sufficient to trigger a full somatic action potential. C , some spontaneous FEPSPs were recorded in this S-neuron prior to the application of the low Ca 2+ –high Mg 2+ solution. These are identified by their irregular amplitudes (see arrow). D , this neuron fired tonically in response to depolarizing current. E , in the presence of the low Ca 2+ –high Mg 2+ solution, removal of hyperpolarizing holding current increased the discharge of process potentials, suggesting that some mechanosensory ion channels may exist close to, or even in the cell soma itself. F , this neuron was an orally projecting uniaxonal filamentous neuron. The calibration bar represents 20 μm. The resting potential of this neuron was −53 mV.

    Techniques Used: Activity Assay, Blocking Assay, Transmission Assay

    26) Product Images from "The functional and molecular studies on involvement of hydrogen sulphide in myometrial activity of non-pregnant buffaloes (Bubalus bubalis)"

    Article Title: The functional and molecular studies on involvement of hydrogen sulphide in myometrial activity of non-pregnant buffaloes (Bubalus bubalis)

    Journal: BMC Veterinary Research

    doi: 10.1186/s12917-017-1288-9

    Representative physiograph recording showing the effect of L-cysteine on myometrial strip of non- pregnant buffaloes in the presence of 100 nM nifedipine ( a ; n = 6) and in Ca 2+ -free RLS (n = 6) on myometrial strips ( b ) from non- pregnant buffaloes
    Figure Legend Snippet: Representative physiograph recording showing the effect of L-cysteine on myometrial strip of non- pregnant buffaloes in the presence of 100 nM nifedipine ( a ; n = 6) and in Ca 2+ -free RLS (n = 6) on myometrial strips ( b ) from non- pregnant buffaloes

    Techniques Used: Stripping Membranes

    27) Product Images from "Characterization of Voltage-Gated Ca2+ Conductances in Layer 5 Neocortical Pyramidal Neurons from Rats"

    Article Title: Characterization of Voltage-Gated Ca2+ Conductances in Layer 5 Neocortical Pyramidal Neurons from Rats

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0004841

    Pharmacological separation of the 5 Ba 2+ current sub-types with Ca 2+ channel blockers. a , Currents evoked by a 50 ms step depolarization to 0 mV from a holding potential of −110 mV before (control) and after application of 10 µM nifedipine. The nifedipine-sensitive current (L-type) was obtained by subtraction. b , c , d and e , Same stimulation protocol as in a . b , 1 µM ω-CgTx GVIA (N-type blocker) was added to the application solution. c , 30 nM SNX-482 (R-type blocker) was added to the application solution. d , 200 nM ω-AgTx IVA (P-type blocker) was added to the application solution. e , the control current was recorded with an application solution containing blockers for L-, N-, R- and P-type. In order to eliminate the remaining current 1 µM ω-CgTx MVIIC (Q-type blocker) was added to the application solution.
    Figure Legend Snippet: Pharmacological separation of the 5 Ba 2+ current sub-types with Ca 2+ channel blockers. a , Currents evoked by a 50 ms step depolarization to 0 mV from a holding potential of −110 mV before (control) and after application of 10 µM nifedipine. The nifedipine-sensitive current (L-type) was obtained by subtraction. b , c , d and e , Same stimulation protocol as in a . b , 1 µM ω-CgTx GVIA (N-type blocker) was added to the application solution. c , 30 nM SNX-482 (R-type blocker) was added to the application solution. d , 200 nM ω-AgTx IVA (P-type blocker) was added to the application solution. e , the control current was recorded with an application solution containing blockers for L-, N-, R- and P-type. In order to eliminate the remaining current 1 µM ω-CgTx MVIIC (Q-type blocker) was added to the application solution.

    Techniques Used: Mass Spectrometry

    28) Product Images from "Simvastatin combined with nifedipine enhances endothelial cell protection by inhibiting ROS generation and activating Akt phosphorylation"

    Article Title: Simvastatin combined with nifedipine enhances endothelial cell protection by inhibiting ROS generation and activating Akt phosphorylation

    Journal: Acta Pharmacologica Sinica

    doi: 10.1038/aps.2010.58

    The concentration-dependent effect of simvastatin combined with nifedipine on eNOS mRNA expression in endothelial cells after hydrogen peroxide-induced injury. Optical densities were obtained after normalization to GAPDH. Data are presented as mean±SEM from three independent experiments. b P
    Figure Legend Snippet: The concentration-dependent effect of simvastatin combined with nifedipine on eNOS mRNA expression in endothelial cells after hydrogen peroxide-induced injury. Optical densities were obtained after normalization to GAPDH. Data are presented as mean±SEM from three independent experiments. b P

    Techniques Used: Concentration Assay, Expressing

    Effect of nifedipine combined with simvastatin on intracellular Ca 2+ in endothelial cells after hydrogen peroxide-induced injury. The change in intracellular Ca 2+ was determined by measuring the fluorescence intensity of the Fluo-3 probe. Cell brightness was analyzed by LaserPix Image software without enhancement. All experiments were performed with at least 40–45 cells. Arbitrary units (au) represent fluorescent intensity corresponding to intracellular Ca 2+ changes. No significant difference. P > 0.05.
    Figure Legend Snippet: Effect of nifedipine combined with simvastatin on intracellular Ca 2+ in endothelial cells after hydrogen peroxide-induced injury. The change in intracellular Ca 2+ was determined by measuring the fluorescence intensity of the Fluo-3 probe. Cell brightness was analyzed by LaserPix Image software without enhancement. All experiments were performed with at least 40–45 cells. Arbitrary units (au) represent fluorescent intensity corresponding to intracellular Ca 2+ changes. No significant difference. P > 0.05.

    Techniques Used: Fluorescence, Software

    The concentration-dependent effect of nifedipine on eNOS protein expressions in endothelial cells after hydrogen peroxide-induced injury. Optical densities were obtained after normalization to β-actin. Data are presented as mean±SEM from three independent experiments. b P
    Figure Legend Snippet: The concentration-dependent effect of nifedipine on eNOS protein expressions in endothelial cells after hydrogen peroxide-induced injury. Optical densities were obtained after normalization to β-actin. Data are presented as mean±SEM from three independent experiments. b P

    Techniques Used: Concentration Assay

    Effect of nifedipine combined with simvastatin on ROS in endothelial cells after hydrogen peroxide-induced injury. Cells were pretreated with 1.0 μmol/L nifedipine for 30 min or 1.0 μmol/L simvastatin for 2 h and 100 μmol/L H 2 O 2 for 30 min. Production of cellular ROS was determined by measuring the fluorescence intensity of the CM-H 2 DCFDA probe at 0 min and 30 min. Cell brightness was measured using LaserPix Image software. Results are presented as mean±SEM for 40−45 cells. Arbitrary units (au) represent fluorescent intensity corresponding to ROS changes. Groups at 0 min: no significant difference. b P
    Figure Legend Snippet: Effect of nifedipine combined with simvastatin on ROS in endothelial cells after hydrogen peroxide-induced injury. Cells were pretreated with 1.0 μmol/L nifedipine for 30 min or 1.0 μmol/L simvastatin for 2 h and 100 μmol/L H 2 O 2 for 30 min. Production of cellular ROS was determined by measuring the fluorescence intensity of the CM-H 2 DCFDA probe at 0 min and 30 min. Cell brightness was measured using LaserPix Image software. Results are presented as mean±SEM for 40−45 cells. Arbitrary units (au) represent fluorescent intensity corresponding to ROS changes. Groups at 0 min: no significant difference. b P

    Techniques Used: Fluorescence, Software

    The concentration-dependent effect of nifedipine on eNOS mRNA expression in endothelial cells after hydrogen peroxide-induced injury. Optical densities were obtained after normalization to GAPDH. Data are presented as mean±SEM from three independent experiments. b P
    Figure Legend Snippet: The concentration-dependent effect of nifedipine on eNOS mRNA expression in endothelial cells after hydrogen peroxide-induced injury. Optical densities were obtained after normalization to GAPDH. Data are presented as mean±SEM from three independent experiments. b P

    Techniques Used: Concentration Assay, Expressing

    The concentration-dependent effect of nifedipine on ROS in endothelial cells after hydrogen peroxide-induced injury. Cells were pretreated with or without nifedipine (0.1, 1.0, and 10.0 μmol/L) and 100 μmol/L H 2 O 2 for 30 min. Production of cellular ROS was determined by measuring the fluorescence intensity of the CM-H 2 DCFDA probe at 0 min and 30 min. Cell brightness was measured using LaserPix Image software. Results are presented as mean±SEM for 35−45 cells. Arbitrary units (au) represent fluorescent intensity corresponding to ROS changes. Groups at 0 min: no significant difference. b P
    Figure Legend Snippet: The concentration-dependent effect of nifedipine on ROS in endothelial cells after hydrogen peroxide-induced injury. Cells were pretreated with or without nifedipine (0.1, 1.0, and 10.0 μmol/L) and 100 μmol/L H 2 O 2 for 30 min. Production of cellular ROS was determined by measuring the fluorescence intensity of the CM-H 2 DCFDA probe at 0 min and 30 min. Cell brightness was measured using LaserPix Image software. Results are presented as mean±SEM for 35−45 cells. Arbitrary units (au) represent fluorescent intensity corresponding to ROS changes. Groups at 0 min: no significant difference. b P

    Techniques Used: Concentration Assay, Fluorescence, Software

    29) Product Images from "AMPA receptor-mediated rapid EPSCs in vestibular calyx afferents"

    Article Title: AMPA receptor-mediated rapid EPSCs in vestibular calyx afferents

    Journal: Journal of Neurophysiology

    doi: 10.1152/jn.00394.2016

    Effects of calcium channel modulators on EPSCs. A and B : EPSCs in the presence of 8 mM Sr 2+ ( A ) followed by the application of nifedipine (20 µM) and 8 mM Sr 2+ ( B ), which resulted in a reduction in EPSC frequency. C : frequency of events increased after nifedipine washout. D : frequency of EPSCs in cells bathed in 8 mM Sr 2+ (control) followed by a combination of Sr 2+ and 20 µM nifedipine decreased from 3.81 ± 0.20 Hz to 1.09 ± 0.25 Hz ( n = 6 cells, t -test, * P
    Figure Legend Snippet: Effects of calcium channel modulators on EPSCs. A and B : EPSCs in the presence of 8 mM Sr 2+ ( A ) followed by the application of nifedipine (20 µM) and 8 mM Sr 2+ ( B ), which resulted in a reduction in EPSC frequency. C : frequency of events increased after nifedipine washout. D : frequency of EPSCs in cells bathed in 8 mM Sr 2+ (control) followed by a combination of Sr 2+ and 20 µM nifedipine decreased from 3.81 ± 0.20 Hz to 1.09 ± 0.25 Hz ( n = 6 cells, t -test, * P

    Techniques Used:

    30) Product Images from "ATP-Sensitive K+ Channel Mediates the Zinc Switch-Off Signal for Glucagon Response During Glucose Deprivation"

    Article Title: ATP-Sensitive K+ Channel Mediates the Zinc Switch-Off Signal for Glucagon Response During Glucose Deprivation

    Journal: Diabetes

    doi: 10.2337/db09-1098

    Glucagon response in the presence and absence of an exogenous zinc switch-off signal during perifusion of STZ-induced diabetic wild-type mouse islets. Islets were pretreated with STZ to kill β-cells, thereby preventing endogenous insulin and zinc secretion. After an initial 30-min perifusion with 16.7 mmol/l glucose and zinc (Zn), at time 0 min the perifusate was changed. Glucagon levels increased significantly only when a perifusate containing no glucose and no zinc, which generated an exogenous zinc switch-off signal to α-cells during glucose deprivation, was begun at 0 min (■, n = 5). Glucagon secretion did not increase if at time 0 min only glucose, but not zinc, was switched off (○, n = 4) or if only zinc but not glucose was switched off (●, n = 4). If at time 0 min nifedipine (NIF) was added to the perifusate, glucagon secretion not only failed to rise but was suppressed despite the presence of the zinc switch-off signal during glucose deprivation (□, n = 3). ▴ at times −10 to 0 min represent the average of experimental values and control values.
    Figure Legend Snippet: Glucagon response in the presence and absence of an exogenous zinc switch-off signal during perifusion of STZ-induced diabetic wild-type mouse islets. Islets were pretreated with STZ to kill β-cells, thereby preventing endogenous insulin and zinc secretion. After an initial 30-min perifusion with 16.7 mmol/l glucose and zinc (Zn), at time 0 min the perifusate was changed. Glucagon levels increased significantly only when a perifusate containing no glucose and no zinc, which generated an exogenous zinc switch-off signal to α-cells during glucose deprivation, was begun at 0 min (■, n = 5). Glucagon secretion did not increase if at time 0 min only glucose, but not zinc, was switched off (○, n = 4) or if only zinc but not glucose was switched off (●, n = 4). If at time 0 min nifedipine (NIF) was added to the perifusate, glucagon secretion not only failed to rise but was suppressed despite the presence of the zinc switch-off signal during glucose deprivation (□, n = 3). ▴ at times −10 to 0 min represent the average of experimental values and control values.

    Techniques Used: Generated

    31) Product Images from "Inhibition of Human Cytochrome P450 3A4 by Cholesterol *"

    Article Title: Inhibition of Human Cytochrome P450 3A4 by Cholesterol *

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.M111.240457

    Inhibitory effects of cholesterol on recombinant P450 3A4. A , nifedipine oxidation (5–200 μ m ); B , quinidine 3 S -hydroxylation (10–300 μ m ); C , quinidine N -oxidation (10–300 μ m ). The data points represent the
    Figure Legend Snippet: Inhibitory effects of cholesterol on recombinant P450 3A4. A , nifedipine oxidation (5–200 μ m ); B , quinidine 3 S -hydroxylation (10–300 μ m ); C , quinidine N -oxidation (10–300 μ m ). The data points represent the

    Techniques Used: Recombinant

    Inhibitory effects of cholesterol in human liver microsomes. A , nifedipine oxidation (5–200 μ m ); B , quinidine 3 S -hydroxylation (10–300 μ m ); C , quinidine N -oxidation (10–300 μ m ). The data points represent
    Figure Legend Snippet: Inhibitory effects of cholesterol in human liver microsomes. A , nifedipine oxidation (5–200 μ m ); B , quinidine 3 S -hydroxylation (10–300 μ m ); C , quinidine N -oxidation (10–300 μ m ). The data points represent

    Techniques Used:

    32) Product Images from "Antihypertensive effects of new dihydropyridine derivatives on phenylephrine-raised blood pressure in rats"

    Article Title: Antihypertensive effects of new dihydropyridine derivatives on phenylephrine-raised blood pressure in rats

    Journal: Research in Pharmaceutical Sciences

    doi: 10.4103/1735-5362.194897

    Baseline and final (A) mean blood pressure (MBP) and (B) heart rate (HR) of all groups. Final measurements were performed after 45 min of phenylephrine (PE) infusion (20 μg/kg/min), or 25 min after injection (0.05 mL) of dimethylsufoxide (DMSO), or 100 μg/kg of nifedipine (NIF) or dihydropyridine derivatives (compounds A, B, C, D, or E). *Significant ( P ≤ 0.05) difference from the final MBP of PE + DMSO-treated group. △ Significant ( P ≤ 0.05) difference from final MBP of PE + nifedipine-treated group.
    Figure Legend Snippet: Baseline and final (A) mean blood pressure (MBP) and (B) heart rate (HR) of all groups. Final measurements were performed after 45 min of phenylephrine (PE) infusion (20 μg/kg/min), or 25 min after injection (0.05 mL) of dimethylsufoxide (DMSO), or 100 μg/kg of nifedipine (NIF) or dihydropyridine derivatives (compounds A, B, C, D, or E). *Significant ( P ≤ 0.05) difference from the final MBP of PE + DMSO-treated group. △ Significant ( P ≤ 0.05) difference from final MBP of PE + nifedipine-treated group.

    Techniques Used: Injection

    Baseline and final (A) mean blood pressure (MBP) and (B) heart rate (HR) of all groups. Final measurements were performed after 45 min of phenylephrine (PE) infusion (20 μg/kg/min), or 25 min after injection of (0.05 mL) of dimethylsufoxide (DMSO), or 300 μg/kg of nifedipine (NIF) or dihydropyridine derivatives (A, B, C, D, or E). *Significant ( P ≤ 0.05) difference from the final MBP of PE + DMSO-treated group. △ Significant ( P ≤ 0.05) difference from final MBP of PE + nifedipine-treated group.
    Figure Legend Snippet: Baseline and final (A) mean blood pressure (MBP) and (B) heart rate (HR) of all groups. Final measurements were performed after 45 min of phenylephrine (PE) infusion (20 μg/kg/min), or 25 min after injection of (0.05 mL) of dimethylsufoxide (DMSO), or 300 μg/kg of nifedipine (NIF) or dihydropyridine derivatives (A, B, C, D, or E). *Significant ( P ≤ 0.05) difference from the final MBP of PE + DMSO-treated group. △ Significant ( P ≤ 0.05) difference from final MBP of PE + nifedipine-treated group.

    Techniques Used: Injection

    Baseline and final (A) mean blood pressure (MBP) and (B) heart rate (HR) of all groups. Final measurements were performed after 45 min of phenylephrine (PE) infusion (20 μg/kg/min), or 25 min after injection of (0.05 mL) of dimethylsufoxide (DMSO), or 1000 ƒÝg/kg of nifedipine (NIF) or dihydropyridine derivatives (A, B, C, D, or E). *Significant ( P ≤ 0.05) difference from the final MBP of PE+DMSO-treated group.ƒ´Significant ( P ≤ 0.05) difference from final MBP of PE + nifedipine-treated group
    Figure Legend Snippet: Baseline and final (A) mean blood pressure (MBP) and (B) heart rate (HR) of all groups. Final measurements were performed after 45 min of phenylephrine (PE) infusion (20 μg/kg/min), or 25 min after injection of (0.05 mL) of dimethylsufoxide (DMSO), or 1000 ƒÝg/kg of nifedipine (NIF) or dihydropyridine derivatives (A, B, C, D, or E). *Significant ( P ≤ 0.05) difference from the final MBP of PE+DMSO-treated group.ƒ´Significant ( P ≤ 0.05) difference from final MBP of PE + nifedipine-treated group

    Techniques Used: Injection

    33) Product Images from "Properties of gastric smooth muscles obtained from mice which lack inositol trisphosphate receptor"

    Article Title: Properties of gastric smooth muscles obtained from mice which lack inositol trisphosphate receptor

    Journal: The Journal of Physiology

    doi: 10.1111/j.1469-7793.2000.00105.x

    Spontaneous activity of antrum smooth muscle cells Spontaneous activities recorded from the antral smooth muscle of wild-type and mutant mice, before ( A and C , respectively) and after ( B and D , respectively) application of nifedipine (1 μM). A and B were recorded from a single cell in the antral region of a 20-day-old wild-type mouse, C and D from a single cell of a 19-day-old mutant mouse. Amplitude of slow wave in wild-type mice: control, 12.3 ± 0.5 mV, n = 16; in nifedipine, 10.8 ± 0.4 mV, n = 19 ( P
    Figure Legend Snippet: Spontaneous activity of antrum smooth muscle cells Spontaneous activities recorded from the antral smooth muscle of wild-type and mutant mice, before ( A and C , respectively) and after ( B and D , respectively) application of nifedipine (1 μM). A and B were recorded from a single cell in the antral region of a 20-day-old wild-type mouse, C and D from a single cell of a 19-day-old mutant mouse. Amplitude of slow wave in wild-type mice: control, 12.3 ± 0.5 mV, n = 16; in nifedipine, 10.8 ± 0.4 mV, n = 19 ( P

    Techniques Used: Activity Assay, Mutagenesis, Mouse Assay

    34) Product Images from "Constriction of Retinal Arterioles to Endothelin-1: Requisite Role of Rho Kinase Independent of Protein Kinase C and L-Type Calcium Channels"

    Article Title: Constriction of Retinal Arterioles to Endothelin-1: Requisite Role of Rho Kinase Independent of Protein Kinase C and L-Type Calcium Channels

    Journal: Investigative Ophthalmology & Visual Science

    doi: 10.1167/iovs.12-9542

    Reversal of ET-1-induced vasoconstriction. Vessels treated with ET-1 (0.1 nM) for 20 minutes constricted to a stable diameter, then were exposed to Ca 2+ -free solution ( n = 6) or treated with 10 μM ( n = 8) or 3 μM ( n = 14) H-1152, nifedipine
    Figure Legend Snippet: Reversal of ET-1-induced vasoconstriction. Vessels treated with ET-1 (0.1 nM) for 20 minutes constricted to a stable diameter, then were exposed to Ca 2+ -free solution ( n = 6) or treated with 10 μM ( n = 8) or 3 μM ( n = 14) H-1152, nifedipine

    Techniques Used:

    Prevention of PDBu-induced vasoconstriction. Vessels with basal tone were pre-treated for 20 minutes with ( A ) Gö-6983 (3 μM, n = 6), ( B ) nifedipine (1 μM, n = 5), or ( C ) H-1152 (3 μM, n = 7), followed by treatment with
    Figure Legend Snippet: Prevention of PDBu-induced vasoconstriction. Vessels with basal tone were pre-treated for 20 minutes with ( A ) Gö-6983 (3 μM, n = 6), ( B ) nifedipine (1 μM, n = 5), or ( C ) H-1152 (3 μM, n = 7), followed by treatment with

    Techniques Used:

    Reversal of PDBu-induced vasoconstriction. Vessels with basal tone were treated with PDBu (0.1 μM) for 20 minutes to produce vasoconstriction, followed by treatment with Gö-6983 (3 μM, n = 5), nifedipine (1 μM, n = 6),
    Figure Legend Snippet: Reversal of PDBu-induced vasoconstriction. Vessels with basal tone were treated with PDBu (0.1 μM) for 20 minutes to produce vasoconstriction, followed by treatment with Gö-6983 (3 μM, n = 5), nifedipine (1 μM, n = 6),

    Techniques Used:

    Prevention of ET-1-induced vasoconstriction. ( A ) Temporal course of vasoconstriction induced by ET-1 (0.1 nM, n = 7) in the presence of basal tone shown as the control response. Pre-treatment of vessels with basal tone with nifedipine (1 μM,
    Figure Legend Snippet: Prevention of ET-1-induced vasoconstriction. ( A ) Temporal course of vasoconstriction induced by ET-1 (0.1 nM, n = 7) in the presence of basal tone shown as the control response. Pre-treatment of vessels with basal tone with nifedipine (1 μM,

    Techniques Used:

    35) Product Images from "Calcium and Protein Kinase C Regulate the Actin Cytoskeleton in the Synaptic Terminal of Retinal Bipolar Cells "

    Article Title: Calcium and Protein Kinase C Regulate the Actin Cytoskeleton in the Synaptic Terminal of Retinal Bipolar Cells

    Journal: The Journal of Cell Biology

    doi:

    Growth of the F-actin network in response to depolarization required Ca 2+ influx. The bar chart plots the mean depth of the actin network in the synaptic pedicle of bipolar cells depolarized for 15 min in Ringer's solution containing 50 mM KCl with 2.5 mM Ca 2+ and either 0.1% DMSO vehicle, 30 μM nifedipine, or 100 μM nifedipine. Also shown is the depth of the F-actin network after depolarization in a solution containing 0 Ca 2+ /1 mM EGTA. Removing external Ca 2+ or blocking L-type Ca 2+ channels prevented growth of the F-actin network.
    Figure Legend Snippet: Growth of the F-actin network in response to depolarization required Ca 2+ influx. The bar chart plots the mean depth of the actin network in the synaptic pedicle of bipolar cells depolarized for 15 min in Ringer's solution containing 50 mM KCl with 2.5 mM Ca 2+ and either 0.1% DMSO vehicle, 30 μM nifedipine, or 100 μM nifedipine. Also shown is the depth of the F-actin network after depolarization in a solution containing 0 Ca 2+ /1 mM EGTA. Removing external Ca 2+ or blocking L-type Ca 2+ channels prevented growth of the F-actin network.

    Techniques Used: Blocking Assay

    36) Product Images from "Ion Fluxes through KCa2 (SK) and Cav1 (L-type) Channels Contribute to Chronoselectivity of Adenosine A1 Receptor-Mediated Actions in Spontaneously Beating Rat Atria"

    Article Title: Ion Fluxes through KCa2 (SK) and Cav1 (L-type) Channels Contribute to Chronoselectivity of Adenosine A1 Receptor-Mediated Actions in Spontaneously Beating Rat Atria

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2016.00045

    Concentration-response curves of R-PIA (0.001–1 μM) on the spontaneously beating rat atria in the absence (Control) and in the presence of voltage-sensitive calcium channels inhibitors: nifedipine (1 μM, A,B), verapamil (1 μM, C,D), and mibefradil (3 μM, E,F) . Drug applications followed the protocol depicted in Figure 2A . The ordinates are percentage of variation of spontaneous contraction rate (chronotropic effect, A,C,E ) and mechanical tension (inotropic effect, B,D,F ) as compared to baseline values obtained before application of R-PIA. The data are expressed as mean ± SEM from an n number of individual experiments. * P
    Figure Legend Snippet: Concentration-response curves of R-PIA (0.001–1 μM) on the spontaneously beating rat atria in the absence (Control) and in the presence of voltage-sensitive calcium channels inhibitors: nifedipine (1 μM, A,B), verapamil (1 μM, C,D), and mibefradil (3 μM, E,F) . Drug applications followed the protocol depicted in Figure 2A . The ordinates are percentage of variation of spontaneous contraction rate (chronotropic effect, A,C,E ) and mechanical tension (inotropic effect, B,D,F ) as compared to baseline values obtained before application of R-PIA. The data are expressed as mean ± SEM from an n number of individual experiments. * P

    Techniques Used: Concentration Assay

    Concentration-response curves of oxotremorine (0.003–3 μM) on the spontaneously beating rat atria in the absence (Control) and in the presence of voltage-sensitive calcium channels inhibitors: nifedipine (1 μM, A,B), verapamil (1 μM, C,D), and mibefradil (3 μM, E,F) . Drug applications followed the protocol depicted in Figure 2A . The ordinates are percentage of variation of spontaneous contraction rate (chronotropic effect, A,C,E ) and mechanical tension (inotropic effect, B,D,F ) as compared to baseline values obtained before application of oxotremorine. The data are expressed as mean ± SEM from an n number of individual experiments.
    Figure Legend Snippet: Concentration-response curves of oxotremorine (0.003–3 μM) on the spontaneously beating rat atria in the absence (Control) and in the presence of voltage-sensitive calcium channels inhibitors: nifedipine (1 μM, A,B), verapamil (1 μM, C,D), and mibefradil (3 μM, E,F) . Drug applications followed the protocol depicted in Figure 2A . The ordinates are percentage of variation of spontaneous contraction rate (chronotropic effect, A,C,E ) and mechanical tension (inotropic effect, B,D,F ) as compared to baseline values obtained before application of oxotremorine. The data are expressed as mean ± SEM from an n number of individual experiments.

    Techniques Used: Concentration Assay

    37) Product Images from "Role of P2X4 receptors in synaptic strengthening in mouse CA1 hippocampal neurons"

    Article Title: Role of P2X4 receptors in synaptic strengthening in mouse CA1 hippocampal neurons

    Journal: The European Journal of Neuroscience

    doi: 10.1111/j.1460-9568.2011.07763.x

    Hyperpolarizing postsynaptic pulses cause a sustained increase in sEPSC amplitude. (A) In wild-type mice (open circles, n = 5), there is an increase of about 50% in the sEPSC amplitude following a train of hyperpolarizing pulses. This is not observed in P2X4 −/− mice (triangles, n = 6). (B) The increase in sEPSCs is not observed when recording electrodes contain BAPTA (10 m m ) (filled circles, n = 3) compared with when they contain EGTA (0.2 m m ) (Control, open circles, n = 5). (C) The increase in sEPSCs is unaffected by nifedipine (10 μ m ) (filled circles, n = 6) compared with control (open circles, n = 5). (D) In wild-type mice (left), non-stationary noise analysis of sEPSCs in control conditions (black circles) and following hyperpolarizing pulses (gray circles) suggests an increase in receptor number underlying this potentiation. In P2X4 −/− mice (right), non-stationary noise analysis of sEPSCs in control conditions (black triangles) and following hyperpolarizing pulses (gray triangles) shows a much smaller rightward shift. Representative record from one experiment.
    Figure Legend Snippet: Hyperpolarizing postsynaptic pulses cause a sustained increase in sEPSC amplitude. (A) In wild-type mice (open circles, n = 5), there is an increase of about 50% in the sEPSC amplitude following a train of hyperpolarizing pulses. This is not observed in P2X4 −/− mice (triangles, n = 6). (B) The increase in sEPSCs is not observed when recording electrodes contain BAPTA (10 m m ) (filled circles, n = 3) compared with when they contain EGTA (0.2 m m ) (Control, open circles, n = 5). (C) The increase in sEPSCs is unaffected by nifedipine (10 μ m ) (filled circles, n = 6) compared with control (open circles, n = 5). (D) In wild-type mice (left), non-stationary noise analysis of sEPSCs in control conditions (black circles) and following hyperpolarizing pulses (gray circles) suggests an increase in receptor number underlying this potentiation. In P2X4 −/− mice (right), non-stationary noise analysis of sEPSCs in control conditions (black triangles) and following hyperpolarizing pulses (gray triangles) shows a much smaller rightward shift. Representative record from one experiment.

    Techniques Used: Mouse Assay

    Depolarizing postsynaptic pulses cause a sustained increase in sEPSC amplitudes. (A) sEPSC amplitudes increase by about 90% in neurons from wild-type mice (open circles, n = 8) and by about 30% in neurons from P2X4 −/− mice (open triangles, n = 9). (B) In wild-type mice, the increase in sEPSCs was unaffected by (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine maleate (MK-801) (10 μ m , open circles, n = 5), but was blocked by nifedipine (10 μ m , filled circles, n = 7). In A and B, the stimulus (upward arrowhead) was a train of 10 depolarizing steps (from −60 to 20 mV, 3 s duration) applied at 6 s intervals. (C) Amplitude histograms before (black line) and after (gray line) the depolarizing pulse stimulus, and cumulative probability plots (inset) show the increase in amplitude observed in wild-type (left) but not in P2X4 −/− (right) mice. (D) For wild-type mice (left), non-stationary noise analysis for control sEPSCs (black symbols) and sEPSCs following depolarizing pulses (gray symbols) shows an increase in variance against the change in mean amplitude, suggesting an increase in receptor number. This is not seen for P2X4 −/− mice (right).
    Figure Legend Snippet: Depolarizing postsynaptic pulses cause a sustained increase in sEPSC amplitudes. (A) sEPSC amplitudes increase by about 90% in neurons from wild-type mice (open circles, n = 8) and by about 30% in neurons from P2X4 −/− mice (open triangles, n = 9). (B) In wild-type mice, the increase in sEPSCs was unaffected by (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine maleate (MK-801) (10 μ m , open circles, n = 5), but was blocked by nifedipine (10 μ m , filled circles, n = 7). In A and B, the stimulus (upward arrowhead) was a train of 10 depolarizing steps (from −60 to 20 mV, 3 s duration) applied at 6 s intervals. (C) Amplitude histograms before (black line) and after (gray line) the depolarizing pulse stimulus, and cumulative probability plots (inset) show the increase in amplitude observed in wild-type (left) but not in P2X4 −/− (right) mice. (D) For wild-type mice (left), non-stationary noise analysis for control sEPSCs (black symbols) and sEPSCs following depolarizing pulses (gray symbols) shows an increase in variance against the change in mean amplitude, suggesting an increase in receptor number. This is not seen for P2X4 −/− mice (right).

    Techniques Used: Mouse Assay

    38) Product Images from "Spontaneous calcium activity in metanephric mesenchymal cells regulates branching morphogenesis in the embryonic kidney"

    Article Title: Spontaneous calcium activity in metanephric mesenchymal cells regulates branching morphogenesis in the embryonic kidney

    Journal: The FASEB Journal

    doi: 10.1096/fj.201802054R

    Calcium stores in the endoplasmic reticulum are the main source for spontaneous calcium activity in MM cells. A ) Application of 30 µM CPA caused almost complete inhibition of calcium transients after an initial rise in intracellular calcium. B – E ) Binary representation of spontaneous calcium transients from 8 randomly selected MM cells exposed to 30 µM CPA ( B ), calcium-free solution (250 µM EGTA) ( C ), 50 µM nifedipine ( D ), and 10 µM BTP-2 ( E ). F , G ) Chronic application of 5 µM CPA from DIV1 to DIV2. H ) Comparison of calcium activity in control and CPA-treated kidneys. Box plot represents the relative number of cells that displayed multiple (≥5) calcium spikes in 5 kidneys in both the control and CPA-treated groups. Statistical significance was calculated by 2-tailed, nonparametric U test ( P
    Figure Legend Snippet: Calcium stores in the endoplasmic reticulum are the main source for spontaneous calcium activity in MM cells. A ) Application of 30 µM CPA caused almost complete inhibition of calcium transients after an initial rise in intracellular calcium. B – E ) Binary representation of spontaneous calcium transients from 8 randomly selected MM cells exposed to 30 µM CPA ( B ), calcium-free solution (250 µM EGTA) ( C ), 50 µM nifedipine ( D ), and 10 µM BTP-2 ( E ). F , G ) Chronic application of 5 µM CPA from DIV1 to DIV2. H ) Comparison of calcium activity in control and CPA-treated kidneys. Box plot represents the relative number of cells that displayed multiple (≥5) calcium spikes in 5 kidneys in both the control and CPA-treated groups. Statistical significance was calculated by 2-tailed, nonparametric U test ( P

    Techniques Used: Activity Assay, Inhibition

    39) Product Images from "An Unsuspected Property of Natriuretic Peptides: Promotion of Calcium-Dependent Catecholamine Release via Protein Kinase G-Mediated Phosphodiesterase Type 3 Inhibition"

    Article Title: An Unsuspected Property of Natriuretic Peptides: Promotion of Calcium-Dependent Catecholamine Release via Protein Kinase G-Mediated Phosphodiesterase Type 3 Inhibition

    Journal: Circulation

    doi: 10.1161/CIRCULATIONAHA.111.059097

    Calcium dependence of the catecholamine-releasing effect of cGMP. A–C. release of endogenous NE from guinea pig heart synaptosomes by 8-Br-cGMP (1 to 100 μM) in the absence (control) and presence of the N- and L-type Ca 2+ channel blockers ω-CTX (100 nM) and nifedipine (5 μM), and of the intracellular Ca 2+ chelator BAPTA (10 μM). D . DA release from NGF-differentiated PC12 cells in the absence (control) and presence of BAPTA (10 μM). Points are mean increases in NE and DA release above basal level (± SEM; n =12 for A and B; n =8 for C; n =4–15 for D). Basal NE and DA levels were 1.42 ± 0.05 and 6.94 ± 0.92 pmol/mg protein, n =32 and 20, respectively. *, P
    Figure Legend Snippet: Calcium dependence of the catecholamine-releasing effect of cGMP. A–C. release of endogenous NE from guinea pig heart synaptosomes by 8-Br-cGMP (1 to 100 μM) in the absence (control) and presence of the N- and L-type Ca 2+ channel blockers ω-CTX (100 nM) and nifedipine (5 μM), and of the intracellular Ca 2+ chelator BAPTA (10 μM). D . DA release from NGF-differentiated PC12 cells in the absence (control) and presence of BAPTA (10 μM). Points are mean increases in NE and DA release above basal level (± SEM; n =12 for A and B; n =8 for C; n =4–15 for D). Basal NE and DA levels were 1.42 ± 0.05 and 6.94 ± 0.92 pmol/mg protein, n =32 and 20, respectively. *, P

    Techniques Used:

    40) Product Images from "A Stem-Cell Based Bioassay to Critically Assess the Pathology of Dysfunctional Neuromuscular Junctions"

    Article Title: A Stem-Cell Based Bioassay to Critically Assess the Pathology of Dysfunctional Neuromuscular Junctions

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0091643

    Endocytosis at NCAM-/- motor terminals is sensitive to inhibition by nifedipine, but insensitive to inhibition by dynasore. ( A ) Representative images of NMJs formed by NCAM +/+ and ( B ) NCAM -/- ESMNs loaded with FM4-64 by 50 Hz stimulation in the presence of nifedipine (50 μM), dynasore (90 μM) or vehicle (DMSO). ( C ) Mean ±SEM FM4-64 fluorescence measured in cultures incubated with vehicle (veh), tetrodotoxin (TTX), dynasore (Dyn), nifedipine (Nif), and agatoxin (ATX). Each value was normalized to the mean vehicle value of each genotype. * P
    Figure Legend Snippet: Endocytosis at NCAM-/- motor terminals is sensitive to inhibition by nifedipine, but insensitive to inhibition by dynasore. ( A ) Representative images of NMJs formed by NCAM +/+ and ( B ) NCAM -/- ESMNs loaded with FM4-64 by 50 Hz stimulation in the presence of nifedipine (50 μM), dynasore (90 μM) or vehicle (DMSO). ( C ) Mean ±SEM FM4-64 fluorescence measured in cultures incubated with vehicle (veh), tetrodotoxin (TTX), dynasore (Dyn), nifedipine (Nif), and agatoxin (ATX). Each value was normalized to the mean vehicle value of each genotype. * P

    Techniques Used: Inhibition, Fluorescence, Incubation

    Chronic treatment of NCAM -/- cultures with nifedipine improves neurotransmission and enhances synaptogenesis. ( A ) Representative sharp electrode intracellular recording traces from 7 DIV NCAM -/- NMJs treated with nifedipine for 10 minutes (acute nifedipine, 50 μM; top) or once a day for 5 days (chronic nifedipine, 5 μM; bottom). ( B ) Mean ±SEM sEPP amplitude following acute or chronic treatment with nifedipine. * P
    Figure Legend Snippet: Chronic treatment of NCAM -/- cultures with nifedipine improves neurotransmission and enhances synaptogenesis. ( A ) Representative sharp electrode intracellular recording traces from 7 DIV NCAM -/- NMJs treated with nifedipine for 10 minutes (acute nifedipine, 50 μM; top) or once a day for 5 days (chronic nifedipine, 5 μM; bottom). ( B ) Mean ±SEM sEPP amplitude following acute or chronic treatment with nifedipine. * P

    Techniques Used:

    Related Articles

    Flow Cytometry:

    Article Title: Sialoglycosylation of RBC in Visceral Leishmaniasis Leads to Enhanced Oxidative Stress, Calpain-Induced Fragmentation of Spectrin and Hemolysis
    Article Snippet: .. To determine the Ca2+ channel type, Fluo 3-loaded RBCVL (2×107 ) in Ringer solution containing Ca2+ (5 mM) were preincubated without or with the indicated doses of ω-agatoxin TK, a spider venom peptide (P/Q-type Ca2+ channel blocker, Calbiochem) or nifedipine (L-type Ca2+ channel blocker, Sigma) for 20 min at 37°C, washed, sensitized with anti-9- O -AcSGP IgG (2.5 µg/ml) as above and analyzed by flow cytometry . .. The Ca2+ concentrations were calculated as [Ca2+ ] = Kd [(F−Fmin )/(Fmax −F)] where Kd is the dissociation constant of the Ca2+ Fluo-3 complex (864 nM at 37°C), F fluorescence of anti-9- O -AcSGP IgG-treated RBC, Fmax the maximal fluorescence intensity with A23187 treated, Fmin corresponds to minimum fluorescence intensity with A23187 and EGTA .

    Transferring:

    Article Title: Sub-cellular Electrical Heterogeneity Revealed by Loose Patch Recording Reflects Differential Localization of Sarcolemmal Ion Channels in Intact Rat Hearts
    Article Snippet: .. In studies with inhibitors of Na+ and Ca2+ channels or NCX, the corresponding blockers, tetrodotoxin (TTX, Sigma, USA), nifedipine (Sigma, USA), or benzyloxyphenyl derivative SN-6 (Tocris, USA), were added to the recording pipette's solution. .. For imaging T-tubule structure, hearts were stained with Di-8-ANEPPS, (Molecular Probes, USA) delivered through perfusion with a Tyrode's solution containing 30 μM of the dye for 30 min at 36–37°C.

    Cytometry:

    Article Title: Sialoglycosylation of RBC in Visceral Leishmaniasis Leads to Enhanced Oxidative Stress, Calpain-Induced Fragmentation of Spectrin and Hemolysis
    Article Snippet: .. To determine the Ca2+ channel type, Fluo 3-loaded RBCVL (2×107 ) in Ringer solution containing Ca2+ (5 mM) were preincubated without or with the indicated doses of ω-agatoxin TK, a spider venom peptide (P/Q-type Ca2+ channel blocker, Calbiochem) or nifedipine (L-type Ca2+ channel blocker, Sigma) for 20 min at 37°C, washed, sensitized with anti-9- O -AcSGP IgG (2.5 µg/ml) as above and analyzed by flow cytometry . .. The Ca2+ concentrations were calculated as [Ca2+ ] = Kd [(F−Fmin )/(Fmax −F)] where Kd is the dissociation constant of the Ca2+ Fluo-3 complex (864 nM at 37°C), F fluorescence of anti-9- O -AcSGP IgG-treated RBC, Fmax the maximal fluorescence intensity with A23187 treated, Fmin corresponds to minimum fluorescence intensity with A23187 and EGTA .

    Blocking Assay:

    Article Title: Endothelial barrier dysfunction induced by nanoparticle exposure through actin remodeling via caveolae/raft-regulated calcium signalling
    Article Snippet: .. To study the effect of nanoparticle exposure on cellular calcium homeostasis, cells were treated with 10 μM Nifedipine (N7634, Sigma), a L-type calcium channel blocker that binds to the N terminals of the calcium channels to block the inward movement of calcium, for 2 hours prior to nanoparticle exposure. .. HUVEC were then exposed to TiO2 , SiO2 , PS NPs, and GNPs for 2 hours, fixed with 4% PFA, and 9 nalysed for actin (Alexa Fluor® 488 Phalloidin, ThermoFisher Scientific) and nucleus (DAPI, D1306, ThermoFisher Scientific).

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 99
    Millipore nifedipine
    Ca 2+ -dependent of PACAP- and Forskolin-induced PRL promoter activity in αT3-1 Cells. αT3-1 cells were transiently transfected with pPRL(−1156).LUC for 6 h by using lipofectamine. After 18 h recovery, the cells were incubated with respective drugs. The cells were treated for 24 hr with increasing doses of ( A ) Ca 2+ ionophore A23187 or ( B ) L-type VSCC activator Bay K8644. Inhibiting extracellular Ca 2+ entry on PRL mRNA expression in carp pituitary cells was examined. In this study, αT3-1 cells over-expressed pPRL(−1156).LUC were treated with ( C ) oPACAP 38 (10 nM, 24 hrs) or ( D ) Forskolin (100 nM, 24 hrs) in the Ca 2+ -free medium (with different doses of EGTA). Further, αT3-1 cells over-expressed pPRL(−1156).LUC were treated with ( E ) oPACAP 38 (10 nM, 24 hrs) or ( F ) Forskolin (100 nM, 24 hrs) in the presence or absence of L-type VSCC blocker <t>nifedipine</t> (10 μM). After drug treatment, cell lysate was prepared for dual-luciferase measurement. Data presented were expressed as percentage of control by conversing the ratio of firefly and renilla luciferase in the same sample. Data presented are expressed as mean ± SEM (n = 4) and different letters denote a significant difference at p
    Nifedipine, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 51 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/nifedipine/product/Millipore
    Average 99 stars, based on 51 article reviews
    Price from $9.99 to $1999.99
    nifedipine - by Bioz Stars, 2021-01
    99/100 stars
      Buy from Supplier


    N/A
    This product is provided as delivered and specified by the issuing Pharmacopoeia All information provided in support of this product including SDS and any product information leaflets have been developed
      Buy from Supplier

    Image Search Results


    Ca 2+ -dependent of PACAP- and Forskolin-induced PRL promoter activity in αT3-1 Cells. αT3-1 cells were transiently transfected with pPRL(−1156).LUC for 6 h by using lipofectamine. After 18 h recovery, the cells were incubated with respective drugs. The cells were treated for 24 hr with increasing doses of ( A ) Ca 2+ ionophore A23187 or ( B ) L-type VSCC activator Bay K8644. Inhibiting extracellular Ca 2+ entry on PRL mRNA expression in carp pituitary cells was examined. In this study, αT3-1 cells over-expressed pPRL(−1156).LUC were treated with ( C ) oPACAP 38 (10 nM, 24 hrs) or ( D ) Forskolin (100 nM, 24 hrs) in the Ca 2+ -free medium (with different doses of EGTA). Further, αT3-1 cells over-expressed pPRL(−1156).LUC were treated with ( E ) oPACAP 38 (10 nM, 24 hrs) or ( F ) Forskolin (100 nM, 24 hrs) in the presence or absence of L-type VSCC blocker nifedipine (10 μM). After drug treatment, cell lysate was prepared for dual-luciferase measurement. Data presented were expressed as percentage of control by conversing the ratio of firefly and renilla luciferase in the same sample. Data presented are expressed as mean ± SEM (n = 4) and different letters denote a significant difference at p

    Journal: Scientific Reports

    Article Title: Grass Carp Prolactin Gene: Structural Characterization and Signal Transduction for PACAP-induced Prolactin Promoter Activity

    doi: 10.1038/s41598-018-23092-0

    Figure Lengend Snippet: Ca 2+ -dependent of PACAP- and Forskolin-induced PRL promoter activity in αT3-1 Cells. αT3-1 cells were transiently transfected with pPRL(−1156).LUC for 6 h by using lipofectamine. After 18 h recovery, the cells were incubated with respective drugs. The cells were treated for 24 hr with increasing doses of ( A ) Ca 2+ ionophore A23187 or ( B ) L-type VSCC activator Bay K8644. Inhibiting extracellular Ca 2+ entry on PRL mRNA expression in carp pituitary cells was examined. In this study, αT3-1 cells over-expressed pPRL(−1156).LUC were treated with ( C ) oPACAP 38 (10 nM, 24 hrs) or ( D ) Forskolin (100 nM, 24 hrs) in the Ca 2+ -free medium (with different doses of EGTA). Further, αT3-1 cells over-expressed pPRL(−1156).LUC were treated with ( E ) oPACAP 38 (10 nM, 24 hrs) or ( F ) Forskolin (100 nM, 24 hrs) in the presence or absence of L-type VSCC blocker nifedipine (10 μM). After drug treatment, cell lysate was prepared for dual-luciferase measurement. Data presented were expressed as percentage of control by conversing the ratio of firefly and renilla luciferase in the same sample. Data presented are expressed as mean ± SEM (n = 4) and different letters denote a significant difference at p

    Article Snippet: Forskolin, H89, MDL12330A, 8-(4-chlorophenylthio)-cAMP (CPT-cAMP), A23187, Bay K8644, nifedipine, verapamil, 2-aminoethoxydiphenyl borate (2-APB), U73122, KN62, KN93, calmidazolium, TPA, GF109203, U0126, PD169316, SP600125, Ly294002, rapamycin and HIMOC were obtained from Calbiochem (San Diego, CA).

    Techniques: Activity Assay, Transfection, Incubation, Expressing, Luciferase

    RGZ induces intracellular calcium mobilization from extra- and intra-cellular sources. (A) Effects of nifedipine (10 mM), thapsigargin (0.1 µM), and GLUT2 sequence-specific silencing with RNAi on 10 µM RGZ-induced intracellular calcium mobilization and (B) insulin secretion (ANOVA within same glucose conditions: n = 4, * P

    Journal: PLoS ONE

    Article Title: PPAR-? Activation Increases Insulin Secretion through the Up-regulation of the Free Fatty Acid Receptor GPR40 in Pancreatic ?-Cells

    doi: 10.1371/journal.pone.0050128

    Figure Lengend Snippet: RGZ induces intracellular calcium mobilization from extra- and intra-cellular sources. (A) Effects of nifedipine (10 mM), thapsigargin (0.1 µM), and GLUT2 sequence-specific silencing with RNAi on 10 µM RGZ-induced intracellular calcium mobilization and (B) insulin secretion (ANOVA within same glucose conditions: n = 4, * P

    Article Snippet: The U-73122 and nifedipine were purchased from Calbiochem (Merk, Nottingham, UK).

    Techniques: Sequencing

    Calcium stores in the endoplasmic reticulum are the main source for spontaneous calcium activity in MM cells. A ) Application of 30 µM CPA caused almost complete inhibition of calcium transients after an initial rise in intracellular calcium. B – E ) Binary representation of spontaneous calcium transients from 8 randomly selected MM cells exposed to 30 µM CPA ( B ), calcium-free solution (250 µM EGTA) ( C ), 50 µM nifedipine ( D ), and 10 µM BTP-2 ( E ). F , G ) Chronic application of 5 µM CPA from DIV1 to DIV2. H ) Comparison of calcium activity in control and CPA-treated kidneys. Box plot represents the relative number of cells that displayed multiple (≥5) calcium spikes in 5 kidneys in both the control and CPA-treated groups. Statistical significance was calculated by 2-tailed, nonparametric U test ( P

    Journal: The FASEB Journal

    Article Title: Spontaneous calcium activity in metanephric mesenchymal cells regulates branching morphogenesis in the embryonic kidney

    doi: 10.1096/fj.201802054R

    Figure Lengend Snippet: Calcium stores in the endoplasmic reticulum are the main source for spontaneous calcium activity in MM cells. A ) Application of 30 µM CPA caused almost complete inhibition of calcium transients after an initial rise in intracellular calcium. B – E ) Binary representation of spontaneous calcium transients from 8 randomly selected MM cells exposed to 30 µM CPA ( B ), calcium-free solution (250 µM EGTA) ( C ), 50 µM nifedipine ( D ), and 10 µM BTP-2 ( E ). F , G ) Chronic application of 5 µM CPA from DIV1 to DIV2. H ) Comparison of calcium activity in control and CPA-treated kidneys. Box plot represents the relative number of cells that displayed multiple (≥5) calcium spikes in 5 kidneys in both the control and CPA-treated groups. Statistical significance was calculated by 2-tailed, nonparametric U test ( P

    Article Snippet: Chemicals Cyclopiazonic acid (CPA), EGTA, and nifedipine were purchased from MilliporeSigma Sweden AB (Stockholm, Sweden).

    Techniques: Activity Assay, Inhibition

    P2d-induces Ca 2+ entry via VDCCs and triggers Ca 2+ release from intracellular stores. (A and B) Effects of different blockers of VDCCs on P2d-induced [Ca 2+ ] i rise and neurite outgrowth, respectively. CTL, no inhibitor added; Nif, nifedipine (10 μM), a blocker of L-type VDCCs; Mib, mibefradil and Pim, pimozide (5 μM both), blockers of T-type VDCCs; and Ctx, conotoxin (2 μM), a blocker of N-type VDCCs. Here and henceforth, 100% indicates neurite outgrowth from cultures stimulated with P2d in the absence of inhibitors, and negCTL indicates neurite outgrowth from nonstimulated cultures. (C) PC12 cells were challenged with P2d either before (left; n = 22) or after (right; n = 18) application of an irreversible inhibitor of Ca 2+ uptake into the ER stores, thapsigargin (TG, 200 nM), in a low Ca 2+ medium. In all fluorometric experiments, n = 20–40.

    Journal: Molecular Biology of the Cell

    Article Title: Neural Cell Adhesion Molecule Induces Intracellular Signaling via Multiple Mechanisms of Ca2+ Homeostasis

    doi: 10.1091/mbc.E05-10-0987

    Figure Lengend Snippet: P2d-induces Ca 2+ entry via VDCCs and triggers Ca 2+ release from intracellular stores. (A and B) Effects of different blockers of VDCCs on P2d-induced [Ca 2+ ] i rise and neurite outgrowth, respectively. CTL, no inhibitor added; Nif, nifedipine (10 μM), a blocker of L-type VDCCs; Mib, mibefradil and Pim, pimozide (5 μM both), blockers of T-type VDCCs; and Ctx, conotoxin (2 μM), a blocker of N-type VDCCs. Here and henceforth, 100% indicates neurite outgrowth from cultures stimulated with P2d in the absence of inhibitors, and negCTL indicates neurite outgrowth from nonstimulated cultures. (C) PC12 cells were challenged with P2d either before (left; n = 22) or after (right; n = 18) application of an irreversible inhibitor of Ca 2+ uptake into the ER stores, thapsigargin (TG, 200 nM), in a low Ca 2+ medium. In all fluorometric experiments, n = 20–40.

    Article Snippet: The receptor tyrosine kinase inhibitors lavendustin A and B; blockers of voltage-gated calcium channels of T-type (flunarizine), L-type (nifedipine), N-type (ω-conotoxin MVIIA), and P/Q-type (ω-agatoxin TK); and a blocker of Ca2+ uptake into the endoplasmic reticulum (ER) stores, thapsigargin, were all from Calbiochem (Merck, Darmstadt, Germany).

    Techniques: CTL Assay