tram34  (Alomone Labs)


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    Structured Review

    Alomone Labs tram34
    Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and <t>apamin+tram34</t> (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P
    Tram34, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    tram34 - by Bioz Stars, 2022-05
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    Images

    1) Product Images from "Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries"

    Article Title: Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0104686

    Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P
    Figure Legend Snippet: Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P

    Techniques Used: Isolation, Mass Spectrometry, Activity Assay

    Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.
    Figure Legend Snippet: Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.

    Techniques Used: Blocking Assay

    IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P
    Figure Legend Snippet: IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P

    Techniques Used: Activity Assay, Mouse Assay

    2) Product Images from "Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries"

    Article Title: Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0104686

    Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P
    Figure Legend Snippet: Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P

    Techniques Used: Isolation, Mass Spectrometry, Activity Assay

    Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.
    Figure Legend Snippet: Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.

    Techniques Used: Blocking Assay

    IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P
    Figure Legend Snippet: IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P

    Techniques Used: Activity Assay, Mouse Assay

    3) Product Images from "Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries"

    Article Title: Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0104686

    Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P
    Figure Legend Snippet: Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P

    Techniques Used: Isolation, Mass Spectrometry, Activity Assay

    Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.
    Figure Legend Snippet: Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.

    Techniques Used: Blocking Assay

    IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P
    Figure Legend Snippet: IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P

    Techniques Used: Activity Assay, Mouse Assay

    4) Product Images from "Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries"

    Article Title: Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0104686

    Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P
    Figure Legend Snippet: Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P

    Techniques Used: Isolation, Mass Spectrometry, Activity Assay

    Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.
    Figure Legend Snippet: Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.

    Techniques Used: Blocking Assay

    IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P
    Figure Legend Snippet: IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P

    Techniques Used: Activity Assay, Mouse Assay

    5) Product Images from "Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries"

    Article Title: Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0104686

    Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P
    Figure Legend Snippet: Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P

    Techniques Used: Isolation, Mass Spectrometry, Activity Assay

    Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.
    Figure Legend Snippet: Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.

    Techniques Used: Blocking Assay

    IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P
    Figure Legend Snippet: IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P

    Techniques Used: Activity Assay, Mouse Assay

    6) Product Images from "Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries"

    Article Title: Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0104686

    Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P
    Figure Legend Snippet: Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P

    Techniques Used: Isolation, Mass Spectrometry, Activity Assay

    Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.
    Figure Legend Snippet: Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.

    Techniques Used: Blocking Assay

    IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P
    Figure Legend Snippet: IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P

    Techniques Used: Activity Assay, Mouse Assay

    7) Product Images from "Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries"

    Article Title: Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0104686

    Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P
    Figure Legend Snippet: Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P

    Techniques Used: Isolation, Mass Spectrometry, Activity Assay

    Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.
    Figure Legend Snippet: Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.

    Techniques Used: Blocking Assay

    IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P
    Figure Legend Snippet: IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P

    Techniques Used: Activity Assay, Mouse Assay

    8) Product Images from "Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries"

    Article Title: Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0104686

    Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P
    Figure Legend Snippet: Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P

    Techniques Used: Isolation, Mass Spectrometry, Activity Assay

    Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.
    Figure Legend Snippet: Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.

    Techniques Used: Blocking Assay

    IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P
    Figure Legend Snippet: IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P

    Techniques Used: Activity Assay, Mouse Assay

    9) Product Images from "Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries"

    Article Title: Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0104686

    Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P
    Figure Legend Snippet: Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P

    Techniques Used: Isolation, Mass Spectrometry, Activity Assay

    Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.
    Figure Legend Snippet: Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.

    Techniques Used: Blocking Assay

    IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P
    Figure Legend Snippet: IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P

    Techniques Used: Activity Assay, Mouse Assay

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    Alomone Labs tram34
    Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and <t>apamin+tram34</t> (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P
    Tram34, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    tram34 - by Bioz Stars, 2022-05
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    92
    Alomone Labs ns1619
    Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or <t>NS1619</t> in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).
    Ns1619, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ns1619/product/Alomone Labs
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ns1619 - by Bioz Stars, 2022-05
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    Image Search Results


    Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P

    Journal: PLoS ONE

    Article Title: Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries

    doi: 10.1371/journal.pone.0104686

    Figure Lengend Snippet: Ovariectomy reduces SK3 channel current density in endothelial cells. A : Representative traces recorded using conventional whole-cell recording on endothelial cells isolated from mesenteric arteries obtained from control mouse. Cells were voltage clamped at their resting membrane potential and a 200 ms voltage ramp from of −80 to +60 mV was delivered to elicit whole cell currents before (control) and after subsequent bath application of apamin (apamin) and apamin+tram34 (tram34). B : SK3 and IK1 current densities isolated from digital subtraction of the traces shown in (A) for control endothelial cells. C : Representative whole-cell current density obtained from ovx endothelial cells. D : SK3 and IK1 current densities isolated from digital subtraction of the traces in (C) for ovx endothelial cells. E : Summarized whole-cell SK3 and IK1 current densities from control (black) and ovx (grey) endothelial cells measured at +30 mV. F : Normalized SK3/IK1 ratios for control (black) and ovx (grey) recordings showing reduced SK3 channel activity in ovx endothelial cells. Asterisk (*) indicates statistical significance from control (P

    Article Snippet: Further, blocking IK1 channels alone with 1 µM tram34 had little effect on control and ovx arteries (control: 2.7±0.9; ovx: 8.0±1.8; n = 8; P > 0.05; ).

    Techniques: Isolation, Mass Spectrometry, Activity Assay

    Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.

    Journal: PLoS ONE

    Article Title: Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries

    doi: 10.1371/journal.pone.0104686

    Figure Lengend Snippet: Reduced ACh-induced vasorelaxation due to decreased SK3 channel contribution in ovx vessels. A : (left panel) Representative force myograph recording showing tension (mN) plotted against time (s) using a mesenteric vessel obtained from control mouse. Addition of 3 µM PE increased tension and 1 µM ACh caused 64% vasorelaxation, normalized to the PE-induced tension. (right panel) Following bath washout, PE was added to pre-contract the vessel ∼50%, followed by the addition of 100 µM L-NAME and 1 µM ACh. L-NAME-induced 61% increase in PE-induced contraction and ACh reduced tension by 34%. B : Representative force myograph trace obtained from an ovx artery. C and D : Summarized results for (A and B) and for other selective inhibitors to block different vasorelaxation pathways to study their ( C ) change in tone and ( D ) contribution to ACh-induced relaxation for both control (black bars) and ovx (grey bars) vessels. C : Change in tone was obtained from tension increase in the presence of inhibitors normalized to the baseline tension (eg. 61% and 34% increase in the presence of L-NAME for control and ovx vessels, respectively, as shown in A and B). D : Contribution to ACh-induced relaxation was calculated from the difference in ACh relaxation before and after inhibitor treatment, normalized to the control (before) ACh relaxation. L-NAME blocks nitric oxide (NO) pathway; indomethacin blocks prostacyclin (PGI 2 ) pathway; apamin (apa) and tram34 (tram) together block the EDH pathway.

    Article Snippet: Further, blocking IK1 channels alone with 1 µM tram34 had little effect on control and ovx arteries (control: 2.7±0.9; ovx: 8.0±1.8; n = 8; P > 0.05; ).

    Techniques: Blocking Assay

    IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P

    Journal: PLoS ONE

    Article Title: Ovariectomy-Induced Reductions in Endothelial SK3 Channel Activity and Endothelium-Dependent Vasorelaxation in Murine Mesenteric Arteries

    doi: 10.1371/journal.pone.0104686

    Figure Lengend Snippet: IK1 channel activity mediates TRPV4-induced vasorelaxation in ovx vessels. A : Summarized results from studies using 500 nM HC067047 (HC), a TRPV4 channel antagonist, on change in tone (left panel) and contribution to ACh-induced relaxation (right panel) using vessels obtained from both control (black) and ovx (grey) mice. B : Summarized results from studies using 300 nM GSK1016790, a TRPV4 channel agonist, on changes to vascular tension in the absence and presence of apamin (apa) and/or tram34 (tram). These studies were performed in the presence of L-NAME and indomethacin. Asterisk (*) denotes statistical significance (P

    Article Snippet: Further, blocking IK1 channels alone with 1 µM tram34 had little effect on control and ovx arteries (control: 2.7±0.9; ovx: 8.0±1.8; n = 8; P > 0.05; ).

    Techniques: Activity Assay, Mouse Assay

    Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).

    Journal: Frontiers in Physiology

    Article Title: Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration

    doi: 10.3389/fphys.2020.00210

    Figure Lengend Snippet: Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).

    Article Snippet: The cells were then subjected to the following treatments after 16 h: IBTX 10 nM; NS1619 10 μM; 5% PL plus heparin (1% v/v); IBTX 10 nM + 5% PL plus heparin (1% v/v); and NS1619 10 μM + 5% PL plus heparin (1% v/v).

    Techniques: Migration, Control Assay, Positive Control