Positive inotropic effects of epigallocatechin-3-gallate (EGCG) involve activation of Na+/H+ and Na+/Ca2+ exchangers

European Journal of Heart Failure
Mario LorenzVerena Stangl

Abstract

There is evidence that the tea catechin epigallocatechin-3-gallate (EGCG) modulates myocardial contractility. However, the underlying mechanisms remain to be determined. To study potential signalling pathways involved in EGCG-induced contractile parameters. EGCG increased fractional shortening in rat cardiac myocytes and enhanced intracellular systolic Ca2+ concentrations. In isolated rat hearts, perfusion with EGCG resulted in significant, dose-dependent increase in peak systolic left ventricular pressure, as well as in contraction and relaxation velocities. Heart rate did not change. Inhibition of the beta1-receptor with metoprolol had no influence on the contractile effects of EGCG. Furthermore, levels of cAMP and phosphorylation of phospholamban did not change with EGCG, indicating that the beta-receptor pathway is not involved. The L-type Ca2+ channel inhibitors, nifedipine and gallopamil, failed to modulate EGCG-induced increase in contractility. However, the myocardial effects and intracellular calcium transients stimulated by EGCG were significantly reduced by the antagonist of the Na+/H+ exchanger (NHE) methyl-N-isobutyl amiloride (MIA), and by blocking of the reverse mode of the Na+/Ca2+ exchanger (NCX) by KB-R7943. T...Continue Reading

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Citations

Mar 12, 2010·Clinical Research in Cardiology : Official Journal of the German Cardiac Society·Derliz MerelesHugo A Katus
Mar 6, 2009·Pflügers Archiv : European journal of physiology·Shih-Rong HsiehYing-Ming Liou
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Nov 1, 2013·The American Journal of Clinical Nutrition·Mario Lorenz

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