Taurine modulates I(Kr) but I(Ks) in guinea-pig ventricular cardiomyocytes.

1. Effects of taurine on the delayed rectifier K+ current (I(K)) in isolated guinea-pig ventricular cardiomyocytes were examined at different intracellular Ca2+ concentration ([Ca2+]i), using whole-cell voltage and current clamp techniques. Experiments were performed at 36 degrees C. 2. Addition of taurine (10-20 mM) decreased the action potential duration (APD) at pCa 8, but increased the APD at pCa 6. Taurine (20 mM) enhanced I(K) at 70 mV by 22.4 +/- 3.1% (n = 6, P < 0.01) at pCa 8, whereas taurine inhibited the I(K) by 27.1 +/- 2.7% (n = 6, P < 0.01) at pCa 6. These responses behaved in a concentration-dependent manner. 3. The I(K) is composed of the rapid and slow components (I(Kr) and I(Ks)). When [Ca2+]i was pCa 6, taurine at 20 mM reduced the tail current of I(Kr) at 70 mV by 16.5 +/- 2.7% (n = 5, P < 0.05) and that of I(Ks) at 70 mV by 27.1 +/- 2.8% (n = 6, P < 0.01). In contrast, at pCa 8, the tail currents of I(Kr) and I(Ks) at 70 mV were enhanced by 13.4 +/- 3.2% (n = 7, P < 0.05) and by 22.4 +/- 3.1% (n = 7, P < 0.01), respectively. The voltages of half-maximum activation (V1/2) for I(Kr) and I(Ks) were not modified by taurine. 4. Addition of E-4031 (5 microM) to taurine had a complete blockade of the tail current of I(Kr), but not I(Ks). The remained tail current (I(Ks)) in the presence of E-4031 (5 microM) was not affected by taurine (20 mM), but was blocked by 293B (30 microM). 5. These results indicate that taurine modulates I(Kr) but not I(Ks), depending on [Ca2+]i, resulting in regulation of the APD.