Abstract
L-type Ca2+ channels play a crucial role in the contraction and the spontaneous activity of the heart. It has been reported that in sinoatrial node cells the L-type Ca2+ channels are derived from not only α1C(Cav1.2) but also α1D (Cav1.3). In this study we have investigated the molecular and electrophysiological properties of L-type Ca2+ channels in porcine sinoatrial node cells, in comparison to those of ventricular cells. In the patch clamp analysis, the L-type Ca2+ current in sinoatrial node cells was activated at more negative potential range than ventricular cells, peaking at 0 mV. Furthermore, the L-type Ca2+ current showed a retarded inactivation with a sustained component between -30 and +30 mV in sinoatrial node cells. Western blot analysis revealed the existence of α1D in sinoatrial node but failed to detect it in ventricles. On the other hand, α1C, which was predominant in ventricles, was only detectable in sinoatrial node. Dihydropyridine binding was examined and showed a KD value of approximately 0.2 nM in both sinoatrial node and ventricles. The results indicate that a1D plays a major role as the L-type Ca2+ current in sinoatrial node cells, and may account for the different kinetics of L-type Ca2+ current between sinoatrial node and ventricular cells. [Jpn J Physiol 54 Suppl:S127 (2004)]