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 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tram34/product/Alomone Labs
    Average 93 stars, based on 6 article reviews
    Price from $9.99 to $1999.99
    tram34 - by Bioz Stars, 2022-08
    93/100 stars

    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

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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
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    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