Enhancement of polydatin on inward rectifier potassium channel current in rat ventricular myocytes.
- Author:
Yan WEI
1
;
Jing-Jing ZHOU
;
Jing YANG
;
Jiao ZHANG
;
Li-Ping ZHANG
;
Yi ZHANG
Author Information
1. Department of Physiology, Hebei Medical University, Shijiazhuang 050017, China; Department of Electrophysiology, Institute of Cardiovascular Research, Luzhou Medical College, Luzhou 646000, China; Hebei Key Laboratory of Medical Biotechnology, Shijiazhuang 050017, China. E-mail: zhyhenry@hotmail.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Anti-Arrhythmia Agents;
pharmacology;
Glucosides;
pharmacology;
Myocytes, Cardiac;
drug effects;
Patch-Clamp Techniques;
Potassium Channels, Inwardly Rectifying;
metabolism;
Rats;
Stilbenes;
pharmacology
- From:
Acta Physiologica Sinica
2013;65(3):285-292
- CountryChina
- Language:English
-
Abstract:
The aim of this study was to investigate the effect of polydatin on transient outward potassium channel current (Ito), steady-state outward potassium channel current (Iss) and inward rectifier potassium channel current (IK1) in ventricular myocytes of rat using the whole-cell patch clamp technique. The results showed: (1) Polydatin (above 10 µmol/L) increased IK1 of ventricular myocytes in a non-concentration dependent manner. (2) Polydatin neither had any effect on Ito peak current of ventricular myocytes, nor changed activation, inactivation and recovery kinetics of Ito. (3) Polydatin had no effect on Iss of ventricular myocytes. These results suggest that polydatin enhances IK1 channel activity, but has no effect on Ito and Iss channels in rat ventricular myocytes, which might be one of the ionic mechanisms for antiarrhythmic effect of polydatin.
