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.