抄録
This paper discusses the development of a cardiac sinoatrial (SA) node pacemaker model. The model successfully reconstructs the experimental action potentials at various concentrations of external Ca2+ and K+. Increasing the amplitude of L-type Ca2+ current (ICaL) prolongs the duration of the action potential and thereby slightly decreases the spontaneous rate. On the other hand, a negative voltage shift of ICaL gating by a few mV markedly increases the spontaneous rate. When the amplitude of sustained inward current (Ist) is increased, the spontaneous rate is increased irrespective of the ICaL amplitude. Increasing [Ca2+]o shortens the action potential and increases the spontaneous rate. When the spontaneous activity is stopped by decreasing ICaL amplitude, the resting potential is nearly constant (−35 mV) over 1–15 mM [K+]o as observed in the experiment. This is because the conductance of the inward background non-selective cation current balances with the outward [K+]o-dependent K+ conductance. The unique role of individual voltage- and time-dependent ion channels is clearly demonstrated and distinguished from that of the background current by calculating an instantaneous zero current potential ("lead potential") during the course of the spontaneous activity.
