Polydatin (PD), a resveratrol glucoside, has recently been suggested to have cardioprotective effects against heart diseases, including ischemia-reperfusion injury and pressure-overload induced ventricular remodeling. The contradictory response could be attributed to PD increasing myofilament Ca2 + sensitivity. Exploring the activities of the two types of Ca2 + channels, L-type Ca2 + channels (LCCs) and ryanodine receptors (RyRs), reveals that PD dose-dependently decreased LCC current (ICa), but increased frequency of spontaneous Ca2 + sparks, the elementary Ca2 + releasing events reflecting RyR activity in intact cells. PD dose-dependently increased the gain of EC coupling. In contrast, PD dose-dependently decreased SR Ca2 + content. Furthermore, PD remarkably negated β-adrenergic receptor (AR) stimulation-induced enhancement of ICa and Ca2 + transients, but did not inhibit β-AR-mediated inotropic effect.
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