H. Sada et al., ACTION-POTENTIAL DURATION-STABILIZING ACTION OF TAURINE IN GUINEA-PIGVENTRICULAR MYOCYTES, Japanese Journal of Pharmacology, 70(4), 1996, pp. 303-312
To examine taurine actions on the rate of repolarization of action pot
entials (AP), L-type Ca2+ (I-Ca), late outward K+ (I-K) 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 I-Ca and I-K, shortened AP durati
on and decelerated the rate (-dV/dt) of terminal repolarization of AP.
In contrast, at a low (0.9 mM) [Ca2+](o), taurine intensified both I-
Ca and I-K, lengthened AP duration and accelerated -dV/dt. However, at
either [Ca2+](o), the resting membrane potential was slightly hyperpo
larized, and the inward rectifier current examined by the ramp-pulse p
rotocol remained unaffected by taurine. Taurine is suggested to mainta
in a stable AP duration by altering the inward Ca2+ and I-K in the opp
osite directions, depending on [Ca2+](o). The relevance of the stabili
zing action of taurine on the AP duration to its reported antiarrhythm
ic efficacies is discussed.