抄録
The activation of a large inward current through the TTX-sensitive Na+ channel (INa) accompanied by Ca2+ current (ICa) activation results in the ventricular action potential. The repolarization of the membrane is mediated by both the inactivation of these two inward current systems and the depolarization-dependent gradual activation of the K+ channels (IKr and IKs). The plateau potential is finally terminated by the repolarization-dependent reopening of the inward rectifier K+ channels (IK1). Various patterns of spontaneous depolarization occur if the inactivation of INa or ICa, the activation of IKr and IKs, or the conductance of IK1 is incomplete. Additionally, a transient inward current via the Na+/Ca2+ exchange is induced by the spontaneous Ca2+ release from the sarcoplasmic reticulum and potentially triggers the extrasystole under the Ca2+ overload condition. These principal mechanisms are modified by the species-dependent expression pattern of ion channels and also by possible intrinsic differences in the channel properties. In the present study, we examine if these mechanisms are applicable to the human ventricular cell models, which is newly developed based on the experimental data obtained from human ventricular myocytes. [J Physiol Sci. 2008;58 Suppl:S80]
