抄録
Atrial myocytes express L-type calcium channel α1 subunits, CaV1.2 and CaV1.3. CaV1.3 activates and inactivates at voltages lower than those of CaV1.2 by approximately -17mV. We have previously reported that CaV1.3 shows slow voltage-dependent inactivation as compared to CaV1.2 and that the carboxy(C)-terminal region of CaV1.3 plays an important role in its slow inactivation kinetics. To elucidate the contribution of CaV1.3 currents in pacemaker potential, we examined ion current kinetics of CaV1.3, CaV1.2 and the chimeric channel CTD in which the C-terminal region of CaV1.2 was replaced by that of CaV1.3 by use of heterologous expression system. The recovery from the inactivation of CaV1.3 was significantly faster than those of CaV1.2 and CTD. The CaV1.3 channel current increased at both diastolic depolarization and repolarization during an action potential (AP). Under repetitive AP clamping with AP waveform of rabbit sino-atrial node at 1Hz, Ca2+ current and Ba2+ current through the three Ca2+ channels were gradually decreased and reached plateau. Interestingly, the availability of CaV1.3 was kept at higher level than that of CaV1.2. The amount of charge influx through CaV1.3 during an AP turned out to be larger than that of CaV1.2. Those results suggest that the unique voltage-dependent kinetics of CaV1.3 increase its contribution in Ca2+ influx and in keeping AP duration. [J Physiol Sci. 2008;58 Suppl:S58]
