To examine taurine actions on the rate of repolarization of action potentials (AP), L-type Ca
2+ (I
ca), late outward K
+ (I
K) and the inward rectifier currents as affected by the external Ca
2+ concentrations ([Ca
2+]
o), whole-cell voltage-clamp and current-clamp experiments were conducted in guinea pig ventricular myocytes. At a high (3.6 mM) [Ca
2+]
o, 10 mM taurine suppressed both I
ca and I
K, shortened AP duration and decelerated the rate (−dV/dt) of terminal repolarization of AP. In contrast, at a low (0.9 mM) [Ca
2+]
o, taurine intensified both I
ca and I
K, lengthened AP duration and accelerated −dV/dt. However, at either [Ca
2+]
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 Ca
2+ and I
K in the opposite directions, depending on [Ca
2+]
o. The relevance of the stabilizing action of taurine on the AP duration to its reported antiarrhythmic efficacies is discussed.
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