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Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes
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| Zeitschriftentitel: | Journal of the American Heart Association |
|---|---|
| Personen und Körperschaften: | , , , , , , , |
| In: | Journal of the American Heart Association, 7, 2018, 3 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Ovid Technologies (Wolters Kluwer Health)
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| Schlagwörter: |
| author_facet |
Lin, Zhenhao Xing, Wenlu Gao, Chuanyu Wang, Xianpei Qi, Datun Dai, Guoyou Zhao, Wen Yan, Ganxin Lin, Zhenhao Xing, Wenlu Gao, Chuanyu Wang, Xianpei Qi, Datun Dai, Guoyou Zhao, Wen Yan, Ganxin |
|---|---|
| author |
Lin, Zhenhao Xing, Wenlu Gao, Chuanyu Wang, Xianpei Qi, Datun Dai, Guoyou Zhao, Wen Yan, Ganxin |
| spellingShingle |
Lin, Zhenhao Xing, Wenlu Gao, Chuanyu Wang, Xianpei Qi, Datun Dai, Guoyou Zhao, Wen Yan, Ganxin Journal of the American Heart Association Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes Cardiology and Cardiovascular Medicine |
| author_sort |
lin, zhenhao |
| spelling |
Lin, Zhenhao Xing, Wenlu Gao, Chuanyu Wang, Xianpei Qi, Datun Dai, Guoyou Zhao, Wen Yan, Ganxin 2047-9980 Ovid Technologies (Wolters Kluwer Health) Cardiology and Cardiovascular Medicine http://dx.doi.org/10.1161/jaha.117.007730 <jats:sec xml:lang="en"> <jats:title>Background</jats:title> <jats:p xml:lang="en"> Vascular endothelial growth factor ( <jats:styled-content style="fixed-case">VEGF</jats:styled-content> ) exerts a number of beneficial effects on ischemic myocardium via its angiogenic properties. However, little is known about whether <jats:styled-content style="fixed-case">VEGF</jats:styled-content> has a direct effect on the electrical properties of cardiomyocytes. In the present study, we investigated the effects of different concentrations of <jats:styled-content style="fixed-case">VEGF</jats:styled-content> on delayed rectifier potassium currents ( <jats:styled-content style="fixed-case"> I <jats:sub>K</jats:sub> </jats:styled-content> ) in guinea pig ventricular myocytes and their effects on action potential ( <jats:styled-content style="fixed-case">AP</jats:styled-content> ) parameters. </jats:p> </jats:sec> <jats:sec xml:lang="en"> <jats:title>Methods and Results</jats:title> <jats:p xml:lang="en"> <jats:styled-content style="fixed-case"> I <jats:sub>K</jats:sub> </jats:styled-content> and <jats:styled-content style="fixed-case">AP</jats:styled-content> were recorded by the whole‐cell patch clamp method in ventricular myocytes. Cells were superfused with control solution or solution containing <jats:styled-content style="fixed-case">VEGF</jats:styled-content> at different concentrations for 10 minutes before recording. Some ventricular myocytes were pretreated with a phosphatidylinositol 3‐kinase inhibitor for 1 hour before the addition of <jats:styled-content style="fixed-case">VEGF</jats:styled-content> . We found that <jats:styled-content style="fixed-case">VEGF</jats:styled-content> inhibited the slowly activating delayed rectifier potassium current ( <jats:styled-content style="fixed-case"> I <jats:sub>K</jats:sub> </jats:styled-content> <jats:sub>s</jats:sub> ) in a concentration‐dependent manner (18.13±1.04 versus 12.73±0.34, n=5, <jats:italic>P</jats:italic> =0.001; 12.73±0.34 versus 9.05±1.20, n=5, <jats:italic>P</jats:italic> =0.036) and prolonged <jats:styled-content style="fixed-case">AP</jats:styled-content> duration (894.5±36.92 versus 746.3±33.71, n=5, <jats:italic>P</jats:italic> =0.021). Wortmannin, a phosphatidylinositol 3‐kinase inhibitor, eliminated these <jats:styled-content style="fixed-case">VEGF</jats:styled-content> ‐induced effects. <jats:styled-content style="fixed-case">VEGF</jats:styled-content> had no significant effect on the rapidly activating delayed rectifier potassium current ( <jats:styled-content style="fixed-case"> I <jats:sub>K</jats:sub> </jats:styled-content> <jats:sub>r</jats:sub> ), resting membrane potential, <jats:styled-content style="fixed-case">AP</jats:styled-content> amplitude, or maximal velocity of depolarization. </jats:p> </jats:sec> <jats:sec xml:lang="en"> <jats:title>Conclusions</jats:title> <jats:p xml:lang="en"> <jats:styled-content style="fixed-case">VEGF</jats:styled-content> inhibited <jats:styled-content style="fixed-case"> I <jats:sub>K</jats:sub> </jats:styled-content> <jats:sub>s</jats:sub> in a concentration‐dependent manner through a phosphatidylinositol 3‐kinase–mediated signaling pathway, leading to <jats:styled-content style="fixed-case">AP</jats:styled-content> prolongation. The results indicate a promising therapeutic potential of <jats:styled-content style="fixed-case">VEGF</jats:styled-content> in prevention of ventricular tachyarrhythmias under conditions of high sympathetic activity and ischemia. </jats:p> </jats:sec> Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes Journal of the American Heart Association |
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lin2018inhibitoryeffectofvascularendothelialgrowthfactorontheslowlyactivatingdelayedrectifierpotassiumcurrentinguineapigventricularmyocytes |
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2018 |
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Ovid Technologies (Wolters Kluwer Health) |
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Journal of the American Heart Association |
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49 |
| title |
Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes |
| title_unstemmed |
Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes |
| title_full |
Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes |
| title_fullStr |
Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes |
| title_full_unstemmed |
Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes |
| title_short |
Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes |
| title_sort |
inhibitory effect of vascular endothelial growth factor on the slowly activating delayed rectifier potassium current in guinea pig ventricular myocytes |
| topic |
Cardiology and Cardiovascular Medicine |
| url |
http://dx.doi.org/10.1161/jaha.117.007730 |
| publishDate |
2018 |
| physical |
|
| description |
<jats:sec xml:lang="en">
<jats:title>Background</jats:title>
<jats:p xml:lang="en">
Vascular endothelial growth factor (
<jats:styled-content style="fixed-case">VEGF</jats:styled-content>
) exerts a number of beneficial effects on ischemic myocardium via its angiogenic properties. However, little is known about whether
<jats:styled-content style="fixed-case">VEGF</jats:styled-content>
has a direct effect on the electrical properties of cardiomyocytes. In the present study, we investigated the effects of different concentrations of
<jats:styled-content style="fixed-case">VEGF</jats:styled-content>
on delayed rectifier potassium currents (
<jats:styled-content style="fixed-case">
I
<jats:sub>K</jats:sub>
</jats:styled-content>
) in guinea pig ventricular myocytes and their effects on action potential (
<jats:styled-content style="fixed-case">AP</jats:styled-content>
) parameters.
</jats:p>
</jats:sec>
<jats:sec xml:lang="en">
<jats:title>Methods and Results</jats:title>
<jats:p xml:lang="en">
<jats:styled-content style="fixed-case">
I
<jats:sub>K</jats:sub>
</jats:styled-content>
and
<jats:styled-content style="fixed-case">AP</jats:styled-content>
were recorded by the whole‐cell patch clamp method in ventricular myocytes. Cells were superfused with control solution or solution containing
<jats:styled-content style="fixed-case">VEGF</jats:styled-content>
at different concentrations for 10 minutes before recording. Some ventricular myocytes were pretreated with a phosphatidylinositol 3‐kinase inhibitor for 1 hour before the addition of
<jats:styled-content style="fixed-case">VEGF</jats:styled-content>
. We found that
<jats:styled-content style="fixed-case">VEGF</jats:styled-content>
inhibited the slowly activating delayed rectifier potassium current (
<jats:styled-content style="fixed-case">
I
<jats:sub>K</jats:sub>
</jats:styled-content>
<jats:sub>s</jats:sub>
) in a concentration‐dependent manner (18.13±1.04 versus 12.73±0.34, n=5,
<jats:italic>P</jats:italic>
=0.001; 12.73±0.34 versus 9.05±1.20, n=5,
<jats:italic>P</jats:italic>
=0.036) and prolonged
<jats:styled-content style="fixed-case">AP</jats:styled-content>
duration (894.5±36.92 versus 746.3±33.71, n=5,
<jats:italic>P</jats:italic>
=0.021). Wortmannin, a phosphatidylinositol 3‐kinase inhibitor, eliminated these
<jats:styled-content style="fixed-case">VEGF</jats:styled-content>
‐induced effects.
<jats:styled-content style="fixed-case">VEGF</jats:styled-content>
had no significant effect on the rapidly activating delayed rectifier potassium current (
<jats:styled-content style="fixed-case">
I
<jats:sub>K</jats:sub>
</jats:styled-content>
<jats:sub>r</jats:sub>
), resting membrane potential,
<jats:styled-content style="fixed-case">AP</jats:styled-content>
amplitude, or maximal velocity of depolarization.
</jats:p>
</jats:sec>
<jats:sec xml:lang="en">
<jats:title>Conclusions</jats:title>
<jats:p xml:lang="en">
<jats:styled-content style="fixed-case">VEGF</jats:styled-content>
inhibited
<jats:styled-content style="fixed-case">
I
<jats:sub>K</jats:sub>
</jats:styled-content>
<jats:sub>s</jats:sub>
in a concentration‐dependent manner through a phosphatidylinositol 3‐kinase–mediated signaling pathway, leading to
<jats:styled-content style="fixed-case">AP</jats:styled-content>
prolongation. The results indicate a promising therapeutic potential of
<jats:styled-content style="fixed-case">VEGF</jats:styled-content>
in prevention of ventricular tachyarrhythmias under conditions of high sympathetic activity and ischemia.
</jats:p>
</jats:sec> |
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| description | <jats:sec xml:lang="en"> <jats:title>Background</jats:title> <jats:p xml:lang="en"> Vascular endothelial growth factor ( <jats:styled-content style="fixed-case">VEGF</jats:styled-content> ) exerts a number of beneficial effects on ischemic myocardium via its angiogenic properties. However, little is known about whether <jats:styled-content style="fixed-case">VEGF</jats:styled-content> has a direct effect on the electrical properties of cardiomyocytes. In the present study, we investigated the effects of different concentrations of <jats:styled-content style="fixed-case">VEGF</jats:styled-content> on delayed rectifier potassium currents ( <jats:styled-content style="fixed-case"> I <jats:sub>K</jats:sub> </jats:styled-content> ) in guinea pig ventricular myocytes and their effects on action potential ( <jats:styled-content style="fixed-case">AP</jats:styled-content> ) parameters. </jats:p> </jats:sec> <jats:sec xml:lang="en"> <jats:title>Methods and Results</jats:title> <jats:p xml:lang="en"> <jats:styled-content style="fixed-case"> I <jats:sub>K</jats:sub> </jats:styled-content> and <jats:styled-content style="fixed-case">AP</jats:styled-content> were recorded by the whole‐cell patch clamp method in ventricular myocytes. Cells were superfused with control solution or solution containing <jats:styled-content style="fixed-case">VEGF</jats:styled-content> at different concentrations for 10 minutes before recording. Some ventricular myocytes were pretreated with a phosphatidylinositol 3‐kinase inhibitor for 1 hour before the addition of <jats:styled-content style="fixed-case">VEGF</jats:styled-content> . We found that <jats:styled-content style="fixed-case">VEGF</jats:styled-content> inhibited the slowly activating delayed rectifier potassium current ( <jats:styled-content style="fixed-case"> I <jats:sub>K</jats:sub> </jats:styled-content> <jats:sub>s</jats:sub> ) in a concentration‐dependent manner (18.13±1.04 versus 12.73±0.34, n=5, <jats:italic>P</jats:italic> =0.001; 12.73±0.34 versus 9.05±1.20, n=5, <jats:italic>P</jats:italic> =0.036) and prolonged <jats:styled-content style="fixed-case">AP</jats:styled-content> duration (894.5±36.92 versus 746.3±33.71, n=5, <jats:italic>P</jats:italic> =0.021). Wortmannin, a phosphatidylinositol 3‐kinase inhibitor, eliminated these <jats:styled-content style="fixed-case">VEGF</jats:styled-content> ‐induced effects. <jats:styled-content style="fixed-case">VEGF</jats:styled-content> had no significant effect on the rapidly activating delayed rectifier potassium current ( <jats:styled-content style="fixed-case"> I <jats:sub>K</jats:sub> </jats:styled-content> <jats:sub>r</jats:sub> ), resting membrane potential, <jats:styled-content style="fixed-case">AP</jats:styled-content> amplitude, or maximal velocity of depolarization. </jats:p> </jats:sec> <jats:sec xml:lang="en"> <jats:title>Conclusions</jats:title> <jats:p xml:lang="en"> <jats:styled-content style="fixed-case">VEGF</jats:styled-content> inhibited <jats:styled-content style="fixed-case"> I <jats:sub>K</jats:sub> </jats:styled-content> <jats:sub>s</jats:sub> in a concentration‐dependent manner through a phosphatidylinositol 3‐kinase–mediated signaling pathway, leading to <jats:styled-content style="fixed-case">AP</jats:styled-content> prolongation. The results indicate a promising therapeutic potential of <jats:styled-content style="fixed-case">VEGF</jats:styled-content> in prevention of ventricular tachyarrhythmias under conditions of high sympathetic activity and ischemia. </jats:p> </jats:sec> |
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| spelling | Lin, Zhenhao Xing, Wenlu Gao, Chuanyu Wang, Xianpei Qi, Datun Dai, Guoyou Zhao, Wen Yan, Ganxin 2047-9980 Ovid Technologies (Wolters Kluwer Health) Cardiology and Cardiovascular Medicine http://dx.doi.org/10.1161/jaha.117.007730 <jats:sec xml:lang="en"> <jats:title>Background</jats:title> <jats:p xml:lang="en"> Vascular endothelial growth factor ( <jats:styled-content style="fixed-case">VEGF</jats:styled-content> ) exerts a number of beneficial effects on ischemic myocardium via its angiogenic properties. However, little is known about whether <jats:styled-content style="fixed-case">VEGF</jats:styled-content> has a direct effect on the electrical properties of cardiomyocytes. In the present study, we investigated the effects of different concentrations of <jats:styled-content style="fixed-case">VEGF</jats:styled-content> on delayed rectifier potassium currents ( <jats:styled-content style="fixed-case"> I <jats:sub>K</jats:sub> </jats:styled-content> ) in guinea pig ventricular myocytes and their effects on action potential ( <jats:styled-content style="fixed-case">AP</jats:styled-content> ) parameters. </jats:p> </jats:sec> <jats:sec xml:lang="en"> <jats:title>Methods and Results</jats:title> <jats:p xml:lang="en"> <jats:styled-content style="fixed-case"> I <jats:sub>K</jats:sub> </jats:styled-content> and <jats:styled-content style="fixed-case">AP</jats:styled-content> were recorded by the whole‐cell patch clamp method in ventricular myocytes. Cells were superfused with control solution or solution containing <jats:styled-content style="fixed-case">VEGF</jats:styled-content> at different concentrations for 10 minutes before recording. Some ventricular myocytes were pretreated with a phosphatidylinositol 3‐kinase inhibitor for 1 hour before the addition of <jats:styled-content style="fixed-case">VEGF</jats:styled-content> . We found that <jats:styled-content style="fixed-case">VEGF</jats:styled-content> inhibited the slowly activating delayed rectifier potassium current ( <jats:styled-content style="fixed-case"> I <jats:sub>K</jats:sub> </jats:styled-content> <jats:sub>s</jats:sub> ) in a concentration‐dependent manner (18.13±1.04 versus 12.73±0.34, n=5, <jats:italic>P</jats:italic> =0.001; 12.73±0.34 versus 9.05±1.20, n=5, <jats:italic>P</jats:italic> =0.036) and prolonged <jats:styled-content style="fixed-case">AP</jats:styled-content> duration (894.5±36.92 versus 746.3±33.71, n=5, <jats:italic>P</jats:italic> =0.021). Wortmannin, a phosphatidylinositol 3‐kinase inhibitor, eliminated these <jats:styled-content style="fixed-case">VEGF</jats:styled-content> ‐induced effects. <jats:styled-content style="fixed-case">VEGF</jats:styled-content> had no significant effect on the rapidly activating delayed rectifier potassium current ( <jats:styled-content style="fixed-case"> I <jats:sub>K</jats:sub> </jats:styled-content> <jats:sub>r</jats:sub> ), resting membrane potential, <jats:styled-content style="fixed-case">AP</jats:styled-content> amplitude, or maximal velocity of depolarization. </jats:p> </jats:sec> <jats:sec xml:lang="en"> <jats:title>Conclusions</jats:title> <jats:p xml:lang="en"> <jats:styled-content style="fixed-case">VEGF</jats:styled-content> inhibited <jats:styled-content style="fixed-case"> I <jats:sub>K</jats:sub> </jats:styled-content> <jats:sub>s</jats:sub> in a concentration‐dependent manner through a phosphatidylinositol 3‐kinase–mediated signaling pathway, leading to <jats:styled-content style="fixed-case">AP</jats:styled-content> prolongation. The results indicate a promising therapeutic potential of <jats:styled-content style="fixed-case">VEGF</jats:styled-content> in prevention of ventricular tachyarrhythmias under conditions of high sympathetic activity and ischemia. </jats:p> </jats:sec> Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes Journal of the American Heart Association |
| spellingShingle | Lin, Zhenhao, Xing, Wenlu, Gao, Chuanyu, Wang, Xianpei, Qi, Datun, Dai, Guoyou, Zhao, Wen, Yan, Ganxin, Journal of the American Heart Association, Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes, Cardiology and Cardiovascular Medicine |
| title | Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes |
| title_full | Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes |
| title_fullStr | Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes |
| title_full_unstemmed | Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes |
| title_short | Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes |
| title_sort | inhibitory effect of vascular endothelial growth factor on the slowly activating delayed rectifier potassium current in guinea pig ventricular myocytes |
| title_unstemmed | Inhibitory Effect of Vascular Endothelial Growth Factor on the Slowly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes |
| topic | Cardiology and Cardiovascular Medicine |
| url | http://dx.doi.org/10.1161/jaha.117.007730 |