Journal: The Journal of General Physiology

Article Title: Ca2+ oscillations, Ca2+ sensitization, and contraction activated by protein kinase C in small airway smooth muscle

doi: 10.1085/jgp.201210876

Figure Lengend Snippet: Effect of extracellular Ca 2+ removal, nifedipine, CPA, and ryanodine on PMA-induced airway SMC twitching. Line scans from airway wall regions obtained from phase-contrast images (similar to that presented in Fig. 1 ) showing airway SMC twitching induced by 10 µM PMA (added 30 min before the recordings started) and their sensitivity to: (A) Ca 2+ -free sHBSS, (B) 10 µM nifedipine, (C) 10 µM CPA, or (D) 25 µM ryanodine. PMA-induced SMC twitching was inhibited by removal of extracellular Ca 2+ , nifedipine, CPA, and ryanodine. Each line scan is representative of three experiments in lung slices from two mice.

Article Snippet: GF-109203X and cyclopiazonic acid (CPA) were from Enzo Life Sciences, whereas Y-27632, nifedipine, and ryanodine were from Abcam.

Techniques: Mouse Assay

Journal: The Journal of General Physiology

Article Title: Ca2+ oscillations, Ca2+ sensitization, and contraction activated by protein kinase C in small airway smooth muscle

doi: 10.1085/jgp.201210876

Figure Lengend Snippet: Effect of extracellular Ca 2+ removal, nifedipine, CPA, and ryanodine on PMA-induced Ca 2+ oscillations. Ca 2+ oscillations in single airway SMCs induced by 10 µM PMA (added 30 min before the recording started) and its inhibition by: (A) superfusion with Ca 2+ -free sHBSS, (B) 10 µM nifedipine, (C) 10 µM CPA, or (D) 25 µM ryanodine. Each trace is representative of four experiments in lung slices from three mice.

Article Snippet: GF-109203X and cyclopiazonic acid (CPA) were from Enzo Life Sciences, whereas Y-27632, nifedipine, and ryanodine were from Abcam.

Techniques: Inhibition, Mouse Assay

Journal: BMC Cardiovascular Disorders

Article Title: AT1-receptor response to non-saturating Ang-II concentrations is amplified by calcium channel blockers

doi: 10.1186/s12872-017-0562-x

Figure Lengend Snippet: Ca V 1.2 regulates AT 1 R signaling in rat aortic smooth muscle cells and ventricular cardiomyocytes. ( a ) Representative [Ca 2+ ] i traces of Oregon Green Bapta 1 loaded rat aortic smooth muscle cells treated with two minutes of 1 nM AngII at times indicated by arrows. Smooth muscle cells were co-treated from 15 min after first AngII exposure throughout the experiment with vehicle (upper), 0.2 μM nifedipine (middle) and 0.9 μM verapamil (lower). (b ) Relative change between first and second response to AngII stimulation for vehicle (open bar), 0.2 μM nifedipine (dark grey bar) and 0.9 μM verapamil (light grey bar). Peaks are calculated as signal above baseline. n = 6 - 7 individual experiments, *: p ≤ 0.05 compared to vehicle. ( c ) Representative [Ca 2+ ] i traces of Oregon Green Bapta 1 loaded rat ventricular myocytes treated with two minutes of 1 nM AngII at times indicated by arrows. Myocytes were co-treated from 15 min after first AngII exposure throughout the experiment with vehicle (upper), 0.2 μM nifedipine (middle) and 0.9 μM verapamil (lower). ( d ) Relative change between first and second response to AngII stimulation for vehicle (open bar), 0.2 μM nifedipine (dark grey bar) and 0.9 μM verapamil (light grey bar). Peaks are calculated as signal above baseline. n = 6 - 10 individual experiments, *: p ≤ 0.05 compared to vehicle, #: p ≤ 0.05 compared to nifedipine

Article Snippet: Nifedipine effects on bradykinin activation of bradykinin B2 receptors were evaluated through comparing signaling strength with or without pretreatment of 100 μM nifedipine on 100 nM bradykinin (Abcam) treatment.

Techniques:

Journal: BMC Cardiovascular Disorders

Article Title: AT1-receptor response to non-saturating Ang-II concentrations is amplified by calcium channel blockers

doi: 10.1186/s12872-017-0562-x

Figure Lengend Snippet: Ca V 1.2 inhibition up-regulates physiological AT 1 R signaling. a Gel image shows a typical RT-PCR of HEK mRNA using primers for Ca V 1.1(left), Ca V 1.2 (center) and Ca V 1.4 (right). As a negative control, each reaction was done omitting the cDNA. Expected band size is, for Ca V 1.1564 bp, Ca V 1.2621 bp and Ca V 1.4501 bp. Gene Ruler 1 kb DNA ladder was used as a size marker. b Quantification of peak [Ca 2+ ] i response to 1 nM AngII exposure alone or in presence of 1 μM or 100 μM nifedipine in Fura Red loaded HEK cells. n = 4 - 6 experiments. **: p ≤ 0.01 compared to 1 nM AngII exposure alone. c Quantification of peak [Ca 2+ ] i response to 1 nM AngII exposure alone or in presence of 2 μM verapamil in Fura Red loaded HEK cells. n = 10 experiments. *: p ≤ 0.05 compared to 1 nM AngII exposure alone. d Representative [Ca 2+ ] i traces from Fura Red loaded HEK cells treated with repeated 1 nM AngII for two minutes at times indicated by the arrows in the presence of 100 μM nifedipine. e Quantification of peak [Ca 2+ ] i response to repeated 1 nM AngII treatment as shown in D. Peaks are calculated as peak signal above baseline. Open bars show 1 nM AngII alone and grey bars show 1 nM AngII in presence of 100 μM nifedipine. n = 4 - 6 experiments. **: p ≤ 0.01 compared to vehicle

Article Snippet: Nifedipine effects on bradykinin activation of bradykinin B2 receptors were evaluated through comparing signaling strength with or without pretreatment of 100 μM nifedipine on 100 nM bradykinin (Abcam) treatment.

Techniques: Inhibition, Reverse Transcription Polymerase Chain Reaction, Negative Control, Marker

Journal: BMC Cardiovascular Disorders

Article Title: AT1-receptor response to non-saturating Ang-II concentrations is amplified by calcium channel blockers

doi: 10.1186/s12872-017-0562-x

Figure Lengend Snippet: G-protein activation is not affected by nifedipine. a The cartoon show the principle of the FRET based assay for detection of G-protein activity. Activity is detected as a decreased FRET signal (increased FRET ratio) when Gαq dissociate from the βγ complex. b Representative FRET ratio traces of HEK cells expressing pGβ-2A-YFP-Gγ2 in response to 2 min exposure to (at arrow) 1 nM AngII in absence (left) or presence of 100 μM nifedipine (right). c Quantification of peak FRET ratio, in response to 1 nM Ang II alone (open bar) and in presence of nifedipine (grey bar) in HEK cells. n = 9 - 11 experiments

Article Snippet: Nifedipine effects on bradykinin activation of bradykinin B2 receptors were evaluated through comparing signaling strength with or without pretreatment of 100 μM nifedipine on 100 nM bradykinin (Abcam) treatment.

Techniques: Activation Assay, Activity Assay, Expressing

Journal: Cell Death & Disease

Article Title: Polybrene induces neural degeneration by bidirectional Ca2+ influx-dependent mitochondrial and ER–mitochondrial dynamics

doi: 10.1038/s41419-018-1009-8

Figure Lengend Snippet: Neuritic degeneration induced by polybrene is dependent on Ca 2+ influx. a , b Ca 2+ influx induced by polybrene was inhibited by EGTA or nifedipine. Neurons were labeled by Fluo-4. a The time course of relative Fluo-4 fluorescence intensity was recorded. b The relative Fluo-4 fluorescence intensity at 3000 s. The fluorescence intensity of Fluo-4 at initiating time was normalized to 100 ( n ≥ 6, *** P

Article Snippet: Briefly, neurons were treated with polybrene for 24 h. For the polybrene treatment with 5 mM EGTA or 50 µM nifedipine (S1808, Selleck), drugs were added simultaneously with polybrene for 12 h. Neurons were observed under a phase-contrast microscope.

Techniques: Labeling, Fluorescence

Journal: PLoS ONE

Article Title: Myosin II ATPase Activity Mediates the Long-Term Potentiation-Induced Exodus of Stable F-Actin Bound by Drebrin A from Dendritic Spines

doi: 10.1371/journal.pone.0085367

Figure Lengend Snippet: Effects of various inhibitors of Ca 2+ entry on DA-actin distribution. Neurons (21 DIV) were incubated in normal medium containing 50 µM APV (A), 20 mM EGTA (B), 20 µM nifedipine (C), or 1 µM thapsigargin (D) for 30 min. The neurons were then stimulated with 100 µM glutamate for an additional 10 min. F-actin images indicate that spines kept their structure during the experiment although their shapes were changed. Scale bars, 5 µm. ( A ) APV pretreatment significantly increased both the drebrin and actin SDRs (n = 30 cells; p

Article Snippet: D-(−)-2-amino-5-phosphonopentanoic acid (APV), bicuculline, (S)-(−)-blebbistatin, (R)-(+)-blebbistatin, thapsigargin and nifedipine were purchased from Tocris (Ellisville, MO, USA).

Techniques: Incubation

Journal: The Journal of General Physiology

Article Title: Calcium-dependent inactivation controls cardiac L-type Ca2+ currents under β-adrenergic stimulation

doi: 10.1085/jgp.201812236

Figure Lengend Snippet: L-type channel inactivation processes upon β-adrenergic stimulus. Representative nifedipine-sensitive current (solid line) elicited by the AP (dashed line) prerecorded from the same cell in a newborn rat cardiomyocyte overexpressing RFP (A), Ca V β 2a (B), CaM wt (D) , or CaM 34 (E). Bar graphs are mean ± SEM ( n = 8) of maximal current normalized by cell capacitance (pA/pF), total time of current normalized by action potential duration (TTC norm ), and the total current integral normalized by cell capacitance (Q total ) from a cardiomyocyte overexpressing RFP (empty bars) and Ca V β 2a (plum bars). CaM wt (empty bars; B) or CaM 34 (blue bars; D). Data are presented as percentages of their respective control situation [RFP for C and CaM wt for F]. *, P

Article Snippet: To accomplish this, APs and nifedipine-sensitive currents were recorded from cardiomyocytes treated with the NCX inhibitor SEA0400 (Tocris, 1 µM).

Techniques: Chick Chorioallantoic Membrane Assay

Journal: The Journal of General Physiology

Article Title: Calcium-dependent inactivation controls cardiac L-type Ca2+ currents under β-adrenergic stimulation

doi: 10.1085/jgp.201812236

Figure Lengend Snippet: L-type calcium current during an AP upon β-adrenergic stimulus. (A and B) Representative nifedipine-sensitive current (solid line) elicited by the AP (dashed line) prerecorded from the same cell in control (A) and isoproterenol-treated (B) newborn rat cardiomyocytes. (C) Bar graph of maximal current normalized by cell capacitance (pA/pF); total time of nifedipine-sensitive current normalized by its APD (TTC norm ); and the total current integral normalized by cell capacitance (Q total ). Data are presented as percentages with respect to the controls. The bar graph shows mean ± SEM; empty bars represent control cardiomyocytes and green bars correspond to isoproterenol-treated cardiomyocytes ( n = 6; *P

Article Snippet: To accomplish this, APs and nifedipine-sensitive currents were recorded from cardiomyocytes treated with the NCX inhibitor SEA0400 (Tocris, 1 µM).

Techniques:

Journal: The Journal of General Physiology

Article Title: Calcium-dependent inactivation controls cardiac L-type Ca2+ currents under β-adrenergic stimulation

doi: 10.1085/jgp.201812236

Figure Lengend Snippet: APs and L-type calcium currents in CDI-impaired cardiomyocytes. (A) Representative AP waveforms from a newborn rat cardiomyocyte overexpressing CaM wt (solid black line) or CaM 34 (dashed blue line). APs were elicited by 2–5 ms depolarizing current injections (100–200 pA) at 1 Hz. The horizontal line indicates zero level. (B) Bar graph of APD estimated at 20% (APD 20 ), 50% (APD 50 ), and 90% (APD 90 ) of the repolarization phase. (C) Phase plot of the normalized first derivative of membrane potential (dV/dt) against membrane potential (V m ) for the APs shown in A. Empty symbols correspond to data from cardiomyocytes overexpressing CaM wt and blue symbols for cardiomyocytes overexpressing CaM 34 . (D) Bar graph of overshoot, threshold potentials, and mean DMPs. (E) Representative nifedipine-sensitive current (solid line) elicited by the AP (dashed line) prerecorded from the same cardiomyocyte overexpressing CaM 34 . (F) Bar graph of maximal current normalized by cell capacitance (pA/pF), total time of nifedipine-sensitive current normalized by its APD (TTC norm ), and the total current integral normalized by cell capacitance (Q total ). Data are shown as percentages with respect to CaM wt -overexpressing cardiomyocytes. Bar graphs are mean ± SEM; empty bars represent cardiomyocytes overexpressing CaM wt , and blue bars correspond to those overexpressing CaM 34 ( n = 7; *, P

Article Snippet: To accomplish this, APs and nifedipine-sensitive currents were recorded from cardiomyocytes treated with the NCX inhibitor SEA0400 (Tocris, 1 µM).

Techniques: Chick Chorioallantoic Membrane Assay, Mass Spectrometry

Journal: The Journal of General Physiology

Article Title: Calcium-dependent inactivation controls cardiac L-type Ca2+ currents under β-adrenergic stimulation

doi: 10.1085/jgp.201812236

Figure Lengend Snippet: Physiological temperature modifies APs and L-type calcium currents in cardiomyocytes. (A) Representative AP waveforms from newborn rat cardiomyocytes at 23°–25°C (black dashed line) or 35°–37°C (brown line). (B) Representative AP waveforms at 35–37°C before (brown line) and after treatment with 1 µM SEA0400 (light blue line). APs were elicited by 2–5 ms depolarizing current injections (100–200 pA) at 1 Hz. (C) Bar graph of the APD percentage change upon isoproterenol treatment, estimated at 20% (APD 20 ), 50% (APD 50 ), and 90% (APD 90 ) of the repolarization phase. (D and E) Representative nifedipine-sensitive current (solid line) elicited by the AP (dashed line) prerecorded from the same cell at 35–37°C in control cardiomyocytes (D) or treated with 1 µM SEA0400 (E). (F) Bar graph of maximal current normalized by cell capacitance (pA/pF), total time of nifedipine-sensitive current normalized by its APD (TTC norm ), and the total current integral normalized by cell capacitance (Q total ). Data are presented as percentages with respect to control cardiomyocytes at 23–25°C. Bar graphs are mean ± SEM; empty bars represent control cardiomyocytes, brown bars correspond to cardiomyocytes at 35–37°C, and light blue bars correspond to cardiomyocytes at 35–37°C treated with 1 µM SEA0400. *, P

Article Snippet: To accomplish this, APs and nifedipine-sensitive currents were recorded from cardiomyocytes treated with the NCX inhibitor SEA0400 (Tocris, 1 µM).

Techniques: Mass Spectrometry

Journal: The Journal of General Physiology

Article Title: Calcium-dependent inactivation controls cardiac L-type Ca2+ currents under β-adrenergic stimulation

doi: 10.1085/jgp.201812236

Figure Lengend Snippet: APs and L-type calcium currents in VDI-impaired newborn rat cardiomyocytes. (A) Representative AP waveforms from a newborn rat cardiomyocyte overexpressing RFP (solid black line) or Ca V β 2a (dashed plum line). APs were elicited by 2–5 ms depolarizing current injections (100–200 pA) at 1 Hz. (B) Bar graph of APD estimated at 20% (APD 20 ), 50% (APD 50 ), and 90% (APD 90 ) of the repolarization phase. (C) Phase plot of the normalized first derivative of membrane potential (dV/dt) against membrane potential (V m ) for the APs shown in A. Cardiomyocytes overexpressing RFP are shown with empty symbols and cardiomyocytes overexpressing Ca V β 2a with plum symbols. (D) Bar graph of overshoot, threshold potentials, and mean DMPs. (E) Representative nifedipine-sensitive current (solid line) elicited by the AP (dashed line) prerecorded from the same cardiomyocyte overexpressing Ca V β 2a . (F) Bar graph of maximal current normalized by cell capacitance (pA/pF), total time of nifedipine-sensitive current normalized by its APD (TTC norm ), and the total current integral normalized by cell capacitance (Q total ). Data are presented as percentages with respect to RFP-transduced cardiomyocytes. Bar graphs are mean ± SEM; empty bars represent cardiomyocytes overexpressing RFP, and plum bars correspond to those overexpressing Ca V β 2a ( n = 6; *, P

Article Snippet: To accomplish this, APs and nifedipine-sensitive currents were recorded from cardiomyocytes treated with the NCX inhibitor SEA0400 (Tocris, 1 µM).

Techniques: Mass Spectrometry

Journal: The Journal of General Physiology

Article Title: Calcium-dependent inactivation controls cardiac L-type Ca2+ currents under β-adrenergic stimulation

doi: 10.1085/jgp.201812236

Figure Lengend Snippet: Role of L-type channel inactivation processes during a simulated AP. (A) Simulated L-type calcium current for the control condition (black line) or for cardiomyocytes with increased L-type channel conductance alone (light gray line) or simultaneously with an increased CDI (violet line) or VDI (pink line). (B) Experimental data showing the maximal nifedipine-sensitive current from control, Ca V β 2a , and CaM 34 before (empty bars) or after (green bars) isoproterenol stimulation. #, P

Article Snippet: To accomplish this, APs and nifedipine-sensitive currents were recorded from cardiomyocytes treated with the NCX inhibitor SEA0400 (Tocris, 1 µM).

Techniques: Chick Chorioallantoic Membrane Assay

Journal: EMBO Reports

Article Title: The Tau/A152T mutation, a risk factor for frontotemporal‐spectrum disorders, leads to NR2B receptor‐mediated excitotoxicity

doi: 10.15252/embr.201541439

Figure Lengend Snippet: hTau AT causes elevation of Ca 2+ levels in CA3 hippocampal neurons at resting state and after membrane depolarization through extrasynaptic NMDA receptors Slices (DIV 15) from control mice were loaded with the Ca 2+ ‐sensitive dye Fura‐2AM. Ratiometric images are presented at baseline and after application of high potassium. Note the increase in intracellular Ca 2+ ([Ca 2+ ] i ) after KCl application. Slices (DIV 15) from hTau AT mice were loaded with the Ca 2+ ‐sensitive dye Fura‐2AM. Ratiometric images at baseline and after application of high potassium chloride in area CA3 are depicted. Note the increase in [Ca 2+ ] i (false color legend) under both conditions in hTau AT slices compared to controls. Electrophysiological example traces (control, black; hTau AT , red) of excitatory postsynaptic field potentials (fEPSP) depict examples of depolarizations that are induced by a single high potassium chloride application in stratum pyramidale (s.p.) of area CA3 in slices in which calcium imaging experiments were conducted. The example depolarization evokes averaged calcium influxes into neurons depicted in the calcium imaging graph. The graph shows the mean of [Ca 2+ ] i changes in response to high KCl in stratum radiatum and stratum pyramidale of area CA3 in Fura‐2AM‐loaded hippocampal slices. After depolarization, [Ca 2+ ] i rises up to ˜600 nM in hTau AT slices (red trace, n = 6 slices, prepared from at least three animals), compared to ˜300 nM in control slices (black trace, n = 6 slices; prepared from at least three animals). Note that even under resting conditions, [Ca 2+ ] i is elevated to ˜120 nM due to hTau AT expression. Quantification of the [Ca 2+ ] i from ratiometric images as depicted in (A) and (B) after background subtraction and selection of regions of interest (10 circles of fixed diameter) in stratum radiatum border to stratum pyramidale of area CA3. Under resting conditions, [Ca 2+ ] i was elevated in transgenic slice cultures (˜120 nM, n = 11) compared to controls (˜80 nM, n = 8). Slices were incubated with one of the following channel blockers: nifedipine (NIF, VGCC; Ctrl n = 8; A152T: n = 7), APV (NMDAR; Ctrl n = 7; A152T n = 8), ifenprodil (IFEN, NMDAR; Ctrl n = 8; A152T n = 7), memantine (MEM, NMDAR; Ctrl/A152T n = 6), 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX; AMPAR; Ctrl n = 8; A152T n = 7)), tetrodotoxin (TTX, VGNaC; Ctrl n = 4; A152T n = 5), tetanus neurotoxin (TeNT, neurotransmitter release; A152T n = 6) or in Ca 2+ ‐free buffer (Ctrl n = 10; A152T n = 7). For each experiment, slice preparations from at least three different mice were used. One‐way ANOVA followed by Tukey's post hoc test; Ctrl: F (7/51) = 3,533; P = 0.0036; A152T: F (8/55) = 5,230; P . Quantification of the maximum peak increase in intracellular calcium after high KCl stimulation. One‐way ANOVA followed by Tukey's post hoc test Ctrl: F (7/45) = 4,080; P = 0.0015; A152T: F (8/53) = 7,580; P

Article Snippet: For Ca2+ imaging, slices were incubated with the following drugs 120 min before and during Fura‐2AM experiments: 20 μM L‐VGCC inhibitor Nifedipine (Tocris Biosciences, Bristol, UK); 100 μM NMDAR blocker APV (Tocris Biosciences, Bristol, UK); 30 μM AMPAR antagonist CNQX (Tocris Biosciences, US); 20 μM NR2B‐containing NMDA receptor antagonist Ifenprodil (Tocris Biosciences, Bristol, UK); 1 μM sodium channel blocker Tetrodotoxin (TTX) or 8 μM NMDA receptor antagonist memantine.

Techniques: Mouse Assay, Imaging, Expressing, Selection, Transgenic Assay, Incubation

Journal: Pharmacology & toxicology

Article Title: Interaction of Dihydropyridine Calcium Channel Agonists and Antagonists with Adenosine Receptors

doi:

Figure Lengend Snippet: Displacement by nifedipine of [ 3 H]-R-PIA and [ 3 H]-XAC bound to membrane receptors. Open symbols [ 3 H]-R-PIA binding (K i app. 4.15 ± 1.37 × 10 −6 , B max app. 653 fmol/mg protein); closed symbols [ 3 H]-XAC (K i app. 1.86 ± 0.42 × 10 −6 M, B max app. 868 fmol/mg protein).

Article Snippet: Methyl 2,6-dimethyl-5-nitro-4-(2-trifluoromethylphenyl) 1,4-dihydropyridine-3-carboxylate, Bay K 8644, and nifedipine were from Bayer AG.

Techniques: Binding Assay

Journal: Molecular Neurodegeneration

Article Title: TRPM8 and Nav1.8 sodium channels are required for transthyretin-induced calcium influx in growth cones of small-diameter TrkA-positive sensory neurons

doi: 10.1186/1750-1326-6-19

Figure Lengend Snippet: Effect of ion channel blockers on L55P TTR-induced calcium influx and analysis of sensitivity to icilin and capsaicin , (A) L55P was applied to DRG growth cones in the presence of VGCC inhibitors (nifedipine, ω-agatoxin IVA, ω-conotoxin GIVA), Na V inhibitors (tetrodotoxin, ambroxol and carbamazepine) and TRP inhibitors (SKF-96365, BCTC). The resulting maximal calcium influx (max ΔF/F 0 ) calculated over the imaging period (7 min) was calculated. (B) Effect of capsaicin (1 μM) and icilin (100 μM) on cytosolic calcium in DRG growth cones in culture. When DRG cultures were pre-treated with ambroxol (5 μM), icilin-induced calcium fluorescence was significantly decreased. All graphs show maximal ΔF/F 0 ± SEM for n = 12-24 growth cones. Significant differences from control values are depicted as: * p

Article Snippet: Pharmacological compounds used in experiments were obtained from the following sources: nifedipine, ω-agatoxin IVA, ω-conotoxin GIVA (Alomone Labs, Israel), SKF-96365 (Tocris, Bristol, UK), [N-(4-tert-butylphenyl)-4-(3-chloropyridin-2-yl)piperazine-1-carboxamide] (BCTC), (ENZO, NY, USA), ambroxol and carbamazepine (Sigma-Aldrich, MO, USA).

Techniques: Imaging, Fluorescence

Journal: Journal of Neurophysiology

Article Title: Modulation of Voltage-Gated Ion Channels in Rat Retinal Ganglion Cells Mediated by Somatostatin Receptor Subtype 4

doi: 10.1152/jn.00098.2010

Figure Lengend Snippet: Intracellular Ca 2+ signaling was reduced by L-803,087 in ganglion cells in retinal flat mount. A : applications of 52 mM K + solution for 30 s depolarized ganglion cells and produced transient increases in intracellular Ca 2+ concentration, measured with the dye fura-2. Traces ( left ) show that, in the absence of drug, the second of paired K + applications produced a smaller peak Ca 2+ signal. On the right , the paired K + pulses, with L-803,087 (100 nM) applied 30 s prior to the second K + application, show greater reduction of the Ca 2+ signal compared with control. Far right panel shows a fluorescent image (stimulated at 380 nm) of a fura-2-containing ganglion cell in the flat-mount retina. B : mean data show amplitudes of the second high K + response expressed as a percentage of first peak in control, L-803,087 (L-803, 100 nM), nifedipine (NIF, 10 μM), and nifedipine plus L-803,087. The mean Ca 2+ transient amplitudes of all 3 drug treatment groups (L-803, NIF, L-803 + NIF) were significantly smaller than those of the control group, but they did not differ among themselves ( n = 21–89 cells/group; * P

Article Snippet: L-803,087 (0.001%) and nifedipine (NIF, 0.1%) were prepared as DMSO stock solutions, frozen at −20°C, and thawed immediately before experiments (numbers in parentheses indicate percentage of DMSO in the final working solution).

Techniques: Produced, Concentration Assay

Journal: The Journal of General Physiology

Article Title: DHPR activation underlies SR Ca2+ release induced by osmotic stress in isolated rat skeletal muscle fibers

doi: 10.1085/jgp.200910191

Figure Lengend Snippet: Cumulative data showing the relative frequencies of LCR events during the peak of the responses to hyperosmotic sucrose, hyperosmotic CaCl 2 , or after transient exposure to a hypoosmotic solution in the absence or presence of nifedipine. ***, statistically significant differences (P

Article Snippet: Stocks of 1 mM fura-2 AM (Biotium Inc.), 1 mM fluo-4 AM (Invitrogen), 1 mM tetracaine, 100 µM nifedipine (MP Biomedicals), 100 µM 9-AC (Alfa Aesar), 200 µM furosemide, or 1 mM bumetanide were dissolved in DMSO.

Techniques:

Journal: The Journal of General Physiology

Article Title: DHPR activation underlies SR Ca2+ release induced by osmotic stress in isolated rat skeletal muscle fibers

doi: 10.1085/jgp.200910191

Figure Lengend Snippet: Representative confocal x-y images (1/second) obtained from fluo-4–loaded FDB fibers before, during, and after exposure to solutions of increased or decreased osmolarity. For each cell, the number of LCR events observed per frame throughout the experiment is indicated in the graph on the right. (A) The application of a hyperosmotic sucrose solution was often associated with a marked elevation of [Ca 2+ ], and LCR was difficult to identify (cell 1). However, where the rise in [Ca 2+ ] was less pronounced, individual LCR events were apparent during the application of sucrose (cell 2). Prior exposure to 100 µM nifedipine, to inhibit the DHPR, prevented LCR upon sucrose exposure (cell 3). (B) The introduction of a hyperosmotic CaCl 2 solution induced LCR (cell 1), which was markedly inhibited in the presence of nifedipine (cell 2). (C) The application of a hypoosmotic (254 mOsm) solution had no apparent effect on [Ca 2+ ] i . However, returning to the isoosmotic solution precipitated LCR events (cell 1). In the presence of nifedipine, transient exposure to a hypoosmotic solution failed to induce LCR (cell 2). Fibers subject to hypoosmotic Tyrode's exposure were initially exposed to isoosmotic Tyrode for 30 s, and then for 2 min to a hypoosmotic before returning to isoosmotic Tyrode's solution for 4 min. Horizontal bar, 20 µm.

Article Snippet: Stocks of 1 mM fura-2 AM (Biotium Inc.), 1 mM fluo-4 AM (Invitrogen), 1 mM tetracaine, 100 µM nifedipine (MP Biomedicals), 100 µM 9-AC (Alfa Aesar), 200 µM furosemide, or 1 mM bumetanide were dissolved in DMSO.

Techniques:

Journal: The Journal of General Physiology

Article Title: DHPR activation underlies SR Ca2+ release induced by osmotic stress in isolated rat skeletal muscle fibers

doi: 10.1085/jgp.200910191

Figure Lengend Snippet: (A) Simultaneous records of E m (top) and the fura-2 fluorescence ratio (bottom) from fibers equilibrated with an isoosmotic solution before transient exposure to solutions made hyperosmotic (404 mOsm) by the addition of sucrose, mannitol, or CaCl 2 , or hypoosmotic (254 mOsm) by decreasing [NaCl] (left-right). (B) The effects of hyperosmotic sucrose or CaCl 2 solutions on E m (top) and the fura-2 fluorescence ratio (bottom) in cells exposed to 100 µM nifedipine to inhibit DHPR activation. (C) Substitution of 100 mM Na + for K + resulted in a sustained depolarization. Thereafter, the introduction of hyperosmotic sucrose solution had no apparent effect on [Ca 2+ ] i , whereas the application of 30 mM caffeine induced a robust [Ca 2+ ] i transient. (D) Accumulated data showing both the relative change in fluorescence ratio (filled bars) and E m (open bars) obtained using the protocols shown in A and B. Bars represent the mean (± SEM), and the number of preparations is indicated in parentheses. **, mean values significantly different to the peak values obtained after the introduction of hyperosmotic sucrose (P

Article Snippet: Stocks of 1 mM fura-2 AM (Biotium Inc.), 1 mM fluo-4 AM (Invitrogen), 1 mM tetracaine, 100 µM nifedipine (MP Biomedicals), 100 µM 9-AC (Alfa Aesar), 200 µM furosemide, or 1 mM bumetanide were dissolved in DMSO.

Techniques: Fluorescence, Activation Assay

Journal: PLoS ONE

Article Title: Nifedipine Promotes the Proliferation and Migration of Breast Cancer Cells

doi: 10.1371/journal.pone.0113649

Figure Lengend Snippet: Selection and validation of the candidate biomarkers related to nifedipine. a) Comparison of gene expression profiles from nude mice tumors with the treatment of nifedipine or CMC-Na. Hierarchical clustering of nude mice tumors with different treatments. A dendrogram of the tumors was shown at the top. The changed genes were also clustered and gene names were on the right. Taken together, there were 51 up-regulated and 18 down-regulated genes found. Among them, there were 35 genes related to cell adhesion and migration. b) Transcript levels of differential genes in nude mice tumors treated with nifedipine or CMC-Na. Nine genes (BRI3, SMOC1, LLGL1, KCNC4, TRIM3, ATP2C1, DLG1, PDE4DIP and COL14A1) were found to have a consistent gain or loss in at least 10 tumor samples. The transcript levels were normalized to the expression of internal 18s rDNA. Data were presented as the mean ± SEM of three independent experiments. Specific comparison between nifedipine groups and control groups, P

Article Snippet: One week after injection, when the breast tumor size reached 100mm3 , nude mice were then fed with nifedipine (4.8 mg/kg) (Yangtze River Pharmaceutical Group), verapamil (4.8 mg/kg) (Central Pharmaceutical Co., Ltd, China) by gauging.

Techniques: Selection, Expressing, Mouse Assay, Migration

Journal: PLoS ONE

Article Title: Nifedipine Promotes the Proliferation and Migration of Breast Cancer Cells

doi: 10.1371/journal.pone.0113649

Figure Lengend Snippet: Inhibition of proliferation, migration and P-Erk of MDA-MB-231 by silencing BRI3 gene expression. a) Effective silencing of BRI3 mRNA in MDA-MB-231 cells after siRNA treatment. BRI3-homo-584 siRNA markedly inhibited BRI3 mRNA expression at 100 nM after transfection for 24h. b) siRNA directed against BRI3 suppressed the facilitation of nifedipine in the proliferation of MDA-MB-231 cells. Data were presented as the mean±SEM of three independent experiments. Specific comparison between nifedipine groups and control groups, P

Article Snippet: One week after injection, when the breast tumor size reached 100mm3 , nude mice were then fed with nifedipine (4.8 mg/kg) (Yangtze River Pharmaceutical Group), verapamil (4.8 mg/kg) (Central Pharmaceutical Co., Ltd, China) by gauging.

Techniques: Inhibition, Migration, Multiple Displacement Amplification, Expressing, Transfection

Journal: PLoS ONE

Article Title: Nifedipine Promotes the Proliferation and Migration of Breast Cancer Cells

doi: 10.1371/journal.pone.0113649

Figure Lengend Snippet: miRNA-524-5p was target of nifedipine and regulated the expression of BRI3. a) Predicted duplex formation between human BRI3 3′-UTR (top) and three miRNA (bottom) including has-miRNA-524-5p, hsa-miR-1224-3p, hsa-miR-1229 by using TargetScan software. b) The expression of miRNA-524-5p decreased in the MDA-MB-231 cells treated with nifedipine for different periods. Results were presented as the mean±SEM of three independent experiments. P

Article Snippet: One week after injection, when the breast tumor size reached 100mm3 , nude mice were then fed with nifedipine (4.8 mg/kg) (Yangtze River Pharmaceutical Group), verapamil (4.8 mg/kg) (Central Pharmaceutical Co., Ltd, China) by gauging.

Techniques: Expressing, Software, Multiple Displacement Amplification

Journal: PLoS ONE

Article Title: Nifedipine Promotes the Proliferation and Migration of Breast Cancer Cells

doi: 10.1371/journal.pone.0113649

Figure Lengend Snippet: The effect of nifedipine on the nude mice in vivo. a) Nude mice were injected with 510 6 MDA-MB-231-GFP cells into the second fat pads to imitate the orthotopic breast cancer inoculation. After one week injection, when the breast tumor size reached 100mm 3 , nude mice were then fed with nifedipine (4.8 mg/kg) or CMC-Na. b) The tumor volume in nude mice described in (a) was measured at the indicated time points and plotted as the mean volume ± SEM; n = 10; P

Article Snippet: One week after injection, when the breast tumor size reached 100mm3 , nude mice were then fed with nifedipine (4.8 mg/kg) (Yangtze River Pharmaceutical Group), verapamil (4.8 mg/kg) (Central Pharmaceutical Co., Ltd, China) by gauging.

Techniques: Mouse Assay, In Vivo, Injection, Multiple Displacement Amplification

Journal: PLoS ONE

Article Title: Nifedipine Promotes the Proliferation and Migration of Breast Cancer Cells

doi: 10.1371/journal.pone.0113649

Figure Lengend Snippet: Nifedipine stimulated the survival and migration of breast cancer cells invitro . a) Different concentrations of nifedipine could stimulate the proliferation of MDA-MB-231 cells. Results represented mean ± SEM of 3 independent experiments. P

Article Snippet: One week after injection, when the breast tumor size reached 100mm3 , nude mice were then fed with nifedipine (4.8 mg/kg) (Yangtze River Pharmaceutical Group), verapamil (4.8 mg/kg) (Central Pharmaceutical Co., Ltd, China) by gauging.

Techniques: Migration, Multiple Displacement Amplification

Journal: PLoS ONE

Article Title: Nifedipine Promotes the Proliferation and Migration of Breast Cancer Cells

doi: 10.1371/journal.pone.0113649

Figure Lengend Snippet: ERK activation in Nifedipine treated breast cancer cells. Phosphorylated Erk (P-Erk) immunoblotting in MDA-MB-231 cells treated with or without nifedipine at the indicated times. The level of phosphorylation was more intensive after treated with nifedipine for 40 minutes. Membranes were reprobed for GADPH for loading control. Gray value was analyzed by the Image J software. Results were represented the mean±SEM. n = 3; 1-way ANOVA. b) Phosphorylated Erk (P-Erk) immunoblotting in tumor tissues from nude mice treated with CMC-Na or nifedipine for 4 weeks. Membranes were reprobed for GADPH for loading control. The results were consistent with that in the MDA-MB-231 cells.

Article Snippet: One week after injection, when the breast tumor size reached 100mm3 , nude mice were then fed with nifedipine (4.8 mg/kg) (Yangtze River Pharmaceutical Group), verapamil (4.8 mg/kg) (Central Pharmaceutical Co., Ltd, China) by gauging.

Techniques: Activation Assay, Multiple Displacement Amplification, Software, Mouse Assay

Journal: PLoS ONE

Article Title: Nifedipine Promotes the Proliferation and Migration of Breast Cancer Cells

doi: 10.1371/journal.pone.0113649

Figure Lengend Snippet: Effect of nifedipine on intracellular calcium concentration in MDA-MB-231 cells. (a) MDA-MB-231 breast cancer cells were loaded with Furo-8 for 30 minutes, as described in “Materials and Methods”. Base-line [Ca 2+ ] i was recorded, followed by sequential additions of 1 uM nifedipine. No obvious changes were observed until the 150th picture was taken (n = 300). (b) No significant increase in [Ca 2+ ] i was observed by increasing the bath [K + ] from 2.5 mM to 90mM until the 150th picture was taken (n = 300).

Article Snippet: One week after injection, when the breast tumor size reached 100mm3 , nude mice were then fed with nifedipine (4.8 mg/kg) (Yangtze River Pharmaceutical Group), verapamil (4.8 mg/kg) (Central Pharmaceutical Co., Ltd, China) by gauging.

Techniques: Concentration Assay, Multiple Displacement Amplification

Journal: The Journal of Neuroscience

Article Title: Metabotropic Modulation of Motoneurons by Scratch-Like Spinal Network Activity

doi: 10.1523/JNEUROSCI.23-25-08625.2003

Figure Lengend Snippet: Motor network activity induces a nifedipine-sensitive increase in excitability of motoneurons. The excitability of motoneurons was tested by injecting suprathreshold-depolarizing current pulses. Evoked episodes of network activity were followed by an

Article Snippet: L-type Ca2+ channels were blocked with nifedipine (20 μ m ; Sigma, St. Louis, MO).

Techniques: Activity Assay

Journal: Channels (Austin, Tex.)

Article Title: Activity and calcium regulate nuclear targeting of the calcium channel β4b subunit in nerve and muscle cells

doi:

Figure Lengend Snippet: Regulation of β 4b nuclear export by co-expressed α 1 subunit, calcium, electrical activity and LMB. Dysgenic myotubes were co-transfected with β 4b -V5 and either GFP-tagged skeletal muscle α 1S or cardiac α 1C subunits, and the percent of cells with nuclear targeting was assessed. (A) examples of myotubes with β 4b -V5 localized in the nuclei (upper) or not (lower); approximate percentages at which each phenotype was observed when coexpressed with GFP-α 1S or GFP-α 1C are indicated (Bar 10 μm). (C) When coexpressed with GFP-α 1C the fraction of cells with β 4b -V5 targeted to the nuclei was reduced to about half of that found in GFP-α 1S expressing cells (n, 1,400 cells, 23 experiments). (B) Representative calcium current traces and current-to-voltage curves of GFP-α 1S and GFP-α 1C show that the cardiac channel activates at lower voltages and conducts several-fold higher current densities as the skeletal muscle channel. (D) application of the calcium channel activator BayK8644 significantly decreased the degree of nuclear targeting in GFP-α 1S and GFP-α 1C expressing cells; the channel blocker nifedipine increased nuclear targeting in GFP-α 1C expressing cells (n, 700 cells, 10 experiments). (E) Depolarization with 80 mM KCl significantly decreased β 4b nuclear targeting in GFP-α 1S expressing cells, whereas blocking spontaneous electric activity with TTX increased nuclear targeting in GFP-α 1C expressing cells (n, 700 cells, 10 experiments). (F) Pretreatment with the CRM-1 inhibitor leptomycin-B (LMB) blocked KCl-mediated nuclear export of β 4b -V5 in GFP-α 1S expressing cells and increased basal nuclear targeting in GFP-α 1C expressing cells (n, 600 cells, 9 experiments; significance *p

Article Snippet: The calcium channel agonist BayK8644 (Sigma) and antagonist nifedipine (Sigma) were applied at a final concentration of 1 μM (in DMSO) for 24 h. Leptomycin B (LMB; 3.5 nM in absolute ethanol; Sigma) was applied for 12 h. Depolarization of myotubes was induced by applying a high K+ tyrode solution (in mM: 65 NaCl, 80 KCl, 2 CaCl2 , 2 MgCl2 , 10 HEPES, 30 glucose, pH7.4) for 5 min prior to fixation.

Techniques: Activity Assay, Transfection, Expressing, Blocking Assay

Journal: The Journal of Physiology

Article Title: Characteristics of 5-HT-containing chemoreceptor cells of the chicken aortic body

doi: 10.1111/j.1469-7793.1999.049ad.x

Figure Lengend Snippet: Voltage-dependent Ba 2+ currents in the epithelioid cells Epithelioid cells were voltage clamped at -70 mV in the presence of tetrodotoxin (0.2 μM) and BaCl 2 (5 mM) instead of CaCl 2 . A , representative recordings of current responses of an epithelioid cell to depolarizing potentials for 30 ms between -60 and +60 mV in 10 mV increments before (Control) and during exposure to CoCl 2 (2 mM), and after its removal (Washout). B , peak inward current-voltage relationships were obtained from the cell before (▪) and during (•) exposure to CoCl 2 , and after its removal (▴). C , effects of nifedipine and ω-conotoxin GVIA on peak Ba 2+ currents in an epithelioid cell. At -70 mV in the presence of tetrodotoxin (0.2 μM), TEA-Cl (5 mM) and BaCl 2 (5 mM), Ba 2+ currents were evoked by depolarizing steps for 15 ms to +10 mV with 20 s intervals. The peak Ba 2+ currents are expressed as percentages of the first Ba 2+ current recorded in the absence of blockers and plotted against time. Nifedipine (1 μM) and ω-conotoxin GVIA (1 μM) were applied during the periods indicated by horizontal lines starting with an arrow. Inset, superimposed current traces with letters corresponding to those in the peak current trace. The dotted line indicates the zero current level.

Article Snippet: The solutions containing veratridine (Sigma), nifedipine (Wako Pure Chemicals, Japan) and Bay K 8644 (Sigma) were prepared by the addition of stock solutions of the drugs dissolved in DMSO.

Techniques: Mass Spectrometry

Journal: PLoS ONE

Article Title: Attenuation of L-Type Ca2+ Channel Expression and Vasomotor Response in the Aorta with Age in Both Wistar-Kyoto and Spontaneously Hypertensive Rats

doi: 10.1371/journal.pone.0088975

Figure Lengend Snippet: Profiles of Relaxation by VDCC Blockers in Both WKY and SHR. Representative traces of nifedipine (A)-, verapamil (C)-, and Trp-His (E)-induced relaxation in PE (1 µM)-contracted aortic rings from both 8- and 40-week WKY and SHR. The relaxation activity was represented as EC 50 values for nifedipine (B), verapamil (D), and Trp-His (F). Results are expressed as the mean ± SEM values (n = 3–7). * P

Article Snippet: Nifedipine was purchased from Nacalai Tesque (Kyoto, Japan).

Techniques: Activity Assay

Journal: Journal of Signal Transduction

Article Title: Upregulation of Voltage-Gated Calcium Channel Cav1.3 in Bovine Somatotropes Treated with Ghrelin

doi: 10.1155/2013/527253

Figure Lengend Snippet: High voltage activation calcium channels' L-type regulation and pathway signaling Ca 2+ /CaM-K II affect GH release in bovine somatotropes. (a) Bar graph illustrating the regulation of hormone release by GHRP-6 (100 nM) applied alone or in the presence of nifedipine (0.5 μ M) a blocker of HVACC L-type. (b) Average amount of GH released in the absences (control) and after treatment with the signaling pathway Ca 2+ /CaM-K II inhibitor KN-62 (10 μ M) alone or in combination with GHRP-6 (100 nM). Each value represents the mean ± SE of determinations performed in triplicate from three independent experiments. The asterisks denote significant differences ( P

Article Snippet: Chemicals Ghrelin (ALX-157-022-M001), tetrodotoxin (BML-NA120-0001), KN-62 (BML-EI230), and nifedipine (ALX-550-091-G005) were purchased from Enzo-Alexis-Biomol (ENZO Life Sciences), GHRP-6 (HOR-298-1) was purchased from ProSpec protein specialist, and D-Lys3-GHRP-6 (G-4535-5MG) was purchased from Sigma (St. Louis, MO).

Techniques: Activation Assay, Chick Chorioallantoic Membrane Assay

Journal: Annals of Clinical and Translational Neurology

Article Title: Drug repositioning in epilepsy reveals novel antiseizure candidates

doi: 10.1002/acn3.703

Figure Lengend Snippet: Larval zebrafish behavioral assays. (A) Doxycycline behavioral assay. The average total distance moved at all speeds (mm) for each treatment group ( n = 7–8). In the first half‐hour behavioral assay (Test 1), larvae were treated with vehicle (−) or doxycycline (Dox). In the second half‐hour behavioral assay (Test 2), larvae were treated with vehicle, Dox, or PTZ . Movement greater than 20 mm/sec is shown in A’. (B) Metformin behavioral assay. The average total distance moved at all speeds (mm) for each treatment group ( n = 30–66). In the first half‐hour behavioral assay, larvae were treated with vehicle or metformin (Met). In the second half‐hour behavioral assay, larvae were treated with vehicle, Met, or PTZ . Movement greater than 20 mm/sec is shown in B’. (C) Nifedipine behavioral assay. The average total distance moved at all speeds (mm) of each treatment group ( n = 38). In the first half‐hour behavioral assay, larvae were treated with vehicle or nifedipine (Nif). In the second half‐hour behavioral assay, larvae were treated with vehicle, Nif, or PTZ . Movement greater than 20 mm/sec is shown in C’. (D) Pyrantel tartrate behavioral assay. The average total distance moved at all speeds (mm) of each treatment group ( n = 38–40). In the first half‐hour behavioral assay, larvae were treated with vehicle or pyrantel tartrate (Pyr). In the second half‐hour behavioral assay, larvae were treated with vehicle, Pyr, or PTZ . Movement greater than 20 mm/sec is shown in D’. Bars represent mean ± SEM . **** P ‐value

Article Snippet: Drug delivery Concentrated stock solutions for pentylenetetrazole (PTZ, Sigma), metformin (Cayman Chemical), doxycycline (Cayman Chemical), nifedipine (Cayman Chemical), and pyrantel tartrate (TargetMol) were made by dissolving each in either ddH2O (PTZ, doxycycline, metformin) or DMSO (nifedipine, pyrantel tartrate).

Techniques: Behavioral Assay, Size-exclusion Chromatography

Journal: The Journal of Cell Biology

Article Title: The L-type voltage-dependent Ca2+ channel EGL-19 controls body wall muscle function in Caenorhabditis elegans

doi: 10.1083/jcb.200203055

Figure Lengend Snippet: Effect on the inward current of the dihydropyridine compound nifedipine and of a substitution of Ba 2 + for Ca 2 + . (A) Currents were obtained on the same cell in response to a voltage pulse to +10 mV from a holding potential of –70 mV. The star indicates the current evoked after addition of 1 μM nifedipine in the external solution. (B) Currents were evoked on the same cell in response to a voltage pulse to +10 mV from a holding potential of –70 mV. The star indicates the current evoked after substitution of 6 mM Ba 2+ for 6 mM Ca 2+ in the external solution.

Article Snippet: Nifedipine (ICN Biomedicals) was dissolved in DMSO at a concentration of 10 mM.

Techniques:

Journal: Pflugers Archiv : European journal of physiology

Article Title: Functional link between muscarinic receptors and large-conductance Ca2+-activated K+ channels in freshly-isolated human detrusor smooth muscle cells

doi: 10.1007/s00424-014-1537-8

Figure Lengend Snippet: mAChR agonist carbachol does not affect the depolarization-induced whole cell steady-state K Ca 1.1 currents under conditions of pharmacological inhibition of the major cellular sources of Ca 2+ for K Ca 1.1 channel activation in freshly-isolated human DSM cells A) Representative original recordings illustrate the depolarization-induced whole cell steady-state K Ca 1.1 currents in the absence (control) and in the presence of carbachol (1 μM). B) The current-voltage relationship curve summarizes the lack of carbachol effects on the whole cell steady-state K Ca 1.1 currents (n=9, N=6; P > 0.05). Steady-state K Ca 1.1 currents were recorded in the presence of ryanodine (30 μM), thapsigargin (100 nM), and nifedipine (1 μM). The bath solution contained 134 mM NaCl, 6 mM KCl, and 2 mM CaCl 2 , and the pipette 110 mM potassium aspartate, 30 mM KCl, 10 mM NaCl, and

Article Snippet: Stock solutions of ryanodine (Enzo Life Sciences, Inc.,NY), nifedipine (Thermo Fisher Scientific, NJ), thapsigargin (MP Biochemicals, LLC, CA), and paxilline (Sigma) were prepared in DMSO or ethanol.

Techniques: Inhibition, Activation Assay, Isolation, Transferring

Journal: Micromachines

Article Title: Tetrafluoroethylene-Propylene Elastomer for Fabrication of Microfluidic Organs-on-Chips Resistant to Drug Absorption

doi: 10.3390/mi10110793

Figure Lengend Snippet: Time-course analysis of drug absorption into PDMS, FEPM, and polystyrene (PS) culture plates (control). Drug concentrations after 0.5, 1, 2, 3, 6, and 24-h incubation of nifedipine, Bay K8644, and coumarin evaluated by high-performance liquid chromatography (HPLC, n = 3, * p

Article Snippet: Three types of drugs, nifedipine (N0528, Tokyo Chemical Industry, Tokyo, Japan), Bay K8644 (B112 Sigma-Aldrich, St. Louis, MO, USA), and coumarin (031-16562, Fujifilm Wako Chemicals, Osaka, Japan), were used to test drug absorption.

Techniques: Incubation, High Performance Liquid Chromatography