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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. However, the mechanisms are poorly understood. This study aims to investigate the direct effects of PD on cardiac Ca(2+) handling and excitation-contraction (EC) coupling to explore the potential role of which in PD-mediated cardioprotection. We found that micromolar PD decreased action potential-elicited Ca(2+) transient, but slightly increased cell shortening. The contradictory response could be attributed to PD increasing myofilament Ca(2+) sensitivity. Exploring the activities of the two types of Ca(2+) channels, L-type Ca(2+) channels (LCCs) and ryanodine receptors (RyRs), reveals that PD dose-dependently decreased LCC current (I(Ca)), but increased frequency of spontaneous Ca(2+) sparks, the elementary Ca(2+) releasing events reflecting RyR activity in intact cells. PD dose-dependently increased the gain of EC coupling. In contrast, PD dose-dependently decreased SR Ca(2+) content. Furthermore, PD remarkably negated β-adrenergic receptor (AR) stimulation-induced enhancement of I(Ca) and Ca(2+) transients, but did not inhibit β-AR-mediated inotropic effect. Inhibition of nitric oxide synthase (NOS) with L-NAME abolished PD regulation of I(Ca) and Ca(2+) spark rate, and significantly inhibited the alteration of Ca(2+) transient and myocyte contractility stimulated by PD. These results collectively indicate that PD modulated cardiac EC coupling mainly by inversely regulating LCC and RyR activity and increasing myofilament Ca(2+) sensitivity through increasing intracrine NO, resulting in suppression of Ca(2+) transient without compromising cardiac contractility. The unique regulation of PD on cardiac EC coupling and responsiveness to β-AR signaling implicates that PD has potential cardioprotective effects against Ca(2+) mishandling related heart diseases.

Titel:	Polydatin modulates Ca(2+) handling, excitation-contraction coupling and β-adrenergic signaling in rat ventricular myocytes.
Autor/in / Beteiligte Person:	Deng, J ; Liu, W ; Wang, Y ; Dong, M ; Zheng, M ; Liu, J
Zeitschrift:	Journal of molecular and cellular cardiology, Jg. 53 (2012-11-01), Heft 5, S. 646-56
Veröffentlichung:	London, New York, Academic Press., 2012
Medientyp:	academicJournal
ISSN:	1095-8584 (electronic)
DOI:	10.1016/j.yjmcc.2012.08.009
Schlagwort:	Adrenergic beta-Agonists pharmacology Animals Calcium metabolism Calcium Channels, L-Type metabolism Calcium Channels, L-Type physiology Cell Survival drug effects Female Male Membrane Potentials Myocardial Contraction Myocytes, Cardiac drug effects Myocytes, Cardiac physiology Myofibrils metabolism Myofibrils physiology NG-Nitroarginine Methyl Ester pharmacology Nitric Oxide metabolism Nitric Oxide physiology Nitric Oxide Synthase antagonists & inhibitors Nitric Oxide Synthase metabolism Patch-Clamp Techniques Rats Rats, Sprague-Dawley Ryanodine Receptor Calcium Release Channel metabolism Sarcoplasmic Reticulum drug effects Sarcoplasmic Reticulum metabolism Cardiotonic Agents pharmacology Excitation Contraction Coupling Glucosides pharmacology Heart Ventricles cytology Myocytes, Cardiac metabolism Receptors, Adrenergic, beta metabolism Stilbenes pharmacology
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, Non-U.S. Gov't Language: English [J Mol Cell Cardiol] 2012 Nov; Vol. 53 (5), pp. 646-56. <i>Date of Electronic Publication: </i>2012 Aug 19. MeSH Terms: Excitation Contraction Coupling* ; Cardiotonic Agents / pharmacology ; Glucosides / pharmacology ; Heart Ventricles / cytology ; Myocytes, Cardiac / metabolism ; Receptors, Adrenergic, beta / metabolism ; Stilbenes / pharmacology ; Adrenergic beta-Agonists / pharmacology ; Animals ; Calcium / metabolism ; Calcium Channels, L-Type / metabolism ; Calcium Channels, L-Type / physiology ; Cell Survival / drug effects ; Female ; Male ; Membrane Potentials ; Myocardial Contraction ; Myocytes, Cardiac / drug effects ; Myocytes, Cardiac / physiology ; Myofibrils / metabolism ; Myofibrils / physiology ; NG-Nitroarginine Methyl Ester / pharmacology ; Nitric Oxide / metabolism ; Nitric Oxide / physiology ; Nitric Oxide Synthase / antagonists & inhibitors ; Nitric Oxide Synthase / metabolism ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Ryanodine Receptor Calcium Release Channel / metabolism ; Sarcoplasmic Reticulum / drug effects ; Sarcoplasmic Reticulum / metabolism Substance Nomenclature: 0 (Adrenergic beta-Agonists) ; 0 (Calcium Channels, L-Type) ; 0 (Cardiotonic Agents) ; 0 (Glucosides) ; 0 (Receptors, Adrenergic, beta) ; 0 (Ryanodine Receptor Calcium Release Channel) ; 0 (Stilbenes) ; 31C4KY9ESH (Nitric Oxide) ; EC 1.14.13.39 (Nitric Oxide Synthase) ; SY7Q814VUP (Calcium) ; V55S2QJN2X (NG-Nitroarginine Methyl Ester) ; XM261C37CQ (polydatin) Entry Date(s): Date Created: 20120828 Date Completed: 20130322 Latest Revision: 20131121 Update Code: 20231215

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Polydatin modulates Ca(2+) handling, excitation-contraction coupling and β-adrenergic signaling in rat ventricular myocytes.