Hideaki Sada (1), Takashi Ban (1) and Nicholas Sperelakis (2)
(1) Department of Pharmacology, School of Medicine, Yamaguchi University, Ube 755, Japan (2) Department of Molecular and Cellular Physiology, School of Medicine, University Cincinnati, Cincinnati, Ohio 45267, U.S.A.
Abstract: To examine taurine actions on the rate of repolarization of action potentials (AP), L-type Ca2+ (ICa), late outward K+ (IK) and the inward rectifier currents as affected by the external Ca2+ concentrations ([Ca2+]o), whole-cell voltage-clamp and current-clamp experiments were conducted in guinea pig ventricular myocytes. At a high (3.6 mM) [Ca2+]o, 10 mM taurine suppressed both ICa and IK, shortened AP duration and decelerated the rate (-dV/dt) of terminal repolarization of AP. In contrast, at a low (0.9 mM) [Ca2+]o, taurine intensified both ICa and IK, lengthened AP duration and accelerated -dV/dt. However, at either [Ca2+]o, the resting membrane potential was slightly hyperpolarized, and the inward rectifier current examined by the ramp-pulse protocol remained unaffected by taurine. Taurine is suggested to maintain a stable AP duration by altering the inward Ca2+ and IK in the opposite directions, depending on [Ca2+]o. The relevance of the stabilizing action of taurine on the AP duration to its reported antiarrhythmic efficacies is discussed.
Keywords:
Taurine, Action potential, Ca2+ channel, K+ channel, Antiarrhythmic action