ReferenceID 3520
Polydatin modulates Ca(2+) handling, excitation-contraction coupling and β-adrenergic signaling in rat ventricular myocytes
J Mol Cell Cardiol
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. Ho
Relationship Network
Interactive first-hop connections across herbs, ingredients, formulas, targets, diseases, symptoms, syndromes, evidence, and monographs.
Click a node to open it in a new tab
Ingredient: 1Reference: 1Links: 1
Arranging relationship network...
Record Fields
Scalar fields from the final reference record.
- Reference Id
- 3520
- Evidence Id
- 20110
- Core Evidence Id
- 20110
- Source Reference Id
- 344
- Herb2 Reference Id
- HBREF000634
- Subject Paper Key
- HBIN040403_22921781
- Pubmed Id
- 22921781
- Doi
- 10.1016/j.yjmcc.2012.08.009
- Paper Title
- Polydatin modulates Ca(2+) handling, excitation-contraction coupling and β-adrenergic signaling in rat ventricular myocytes
- Paper Abstract
- 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.
- Journal
- J Mol Cell Cardiol
- Publish Year
- 2012
- Experiment Subject
- Experiment Type
- Others
- Phenotype Related
- Heart Diseases
- Paper Title Cn
- Paper Title En
- Polydatin modulates Ca(2+) handling, excitation-contraction coupling and β-adrenergic signaling in rat ventricular myocytes
- Bilingual Status
- semi_complete