Effect of polydatin on action potential in ventricular papillary muscle of rat and the underlying ionic mechanism.
- Author:
Li-Ping ZHANG
1
;
Yan WEI
;
Sheng-Li SONG
;
Ming CHENG
;
Yi ZHANG
Author Information
1. Department of Physiology, Hebei Medical University, Shijiazhuang 050017, China. zhyhenry@hotmail.com
- Publication Type:Journal Article
- MeSH:
Action Potentials;
drug effects;
Animals;
Calcium Channels, L-Type;
metabolism;
Drugs, Chinese Herbal;
pharmacology;
Glucosides;
pharmacology;
Heart Ventricles;
cytology;
KATP Channels;
metabolism;
Male;
Papillary Muscles;
metabolism;
physiology;
Rats;
Rats, Sprague-Dawley;
Stilbenes;
pharmacology
- From:
Acta Physiologica Sinica
2011;63(1):48-54
- CountryChina
- Language:English
-
Abstract:
It is proved that polydatin has cardioprotection against ischemia-induced arrhythmia, but the electrophysiological mechanism is not clear. The aim of the present study was to investigate the effect of polydatin on action potential (AP) in ventricular papillary muscle and the underlying ionic mechanism in rat using intracellular recording and whole-cell patch clamp techniques. The results showed: (1) In normal papillary muscles, polydatin (50 and 100 µmol/L) shortened duration of 50% repolarization (APD(50)) and duration of 90% repolarization (APD(90)) in a concentration-dependent manner (P<0.01). But polydatin had no effects on resting potential (RP), overshoot (OS), amplitude of action potential (APA) and maximal rate of depolarization in phase 0 (V(max)) in normal papillary muscles (P>0.05). (2) In partially depolarized papillary muscles, polydatin (50 µmol/L) not only shortened APD(50) and APD(90) (P<0.05), but also decreased OS, APA and V(max) (P<0.05). (3) After pretreatment with glibenclamide (10 µmol/L), an ATP-sensitive K(+) channel blocker, the electrophysiological effect of polydatin (50 µmol/L) was partially inhibited. (4) Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME, 1 mmol/L), a nitric oxide (NO) synthase inhibitor, failed to abolish the effect of polydatin (50 µmol/L) on AP. (5) Polydatin (25, 50, 75 and 100 µmol/L) decreased L-type Ca(2+) current in ventricular myocytes in a concentration-dependent manner (P<0.05). (6) Polydatin (50 µmol/L) increased ATP-sensitive K(+) current in ventricular myocytes (P<0.05). The results suggest that polydatin can shorten the repolarization of AP in normal papillary muscle and inhibit AP in partially depolarized papillary muscle, which might be related to the blocking of L-type Ca(2+) channel and the opening of ATP-sensitive K(+) channel.
