[Transmembrane inward currents during excitation of the heart (author's transl)]

Abstract

During excitation of the myocardial cell 2 transmembrane inward currents occur. The initial fast Na current is responsible for the upstroke of the normal action potential. The slow inward current is triggered at a threshold potential of about -40 mV and causes the plateau phase of action potential. Under physiological conditions Ca ions are the main charge carriers of the slow inward current. Both inward currents are mediated by 2 membrane channels which are independent from each other. The normal excitability of the myocardial cell depends upon the availability of the fast Na channel but the transmembrane Ca supply will be determined by the Ca conductance of the slow channel. After inactivation of the fast Na channel the excitability of the myocardial cell does not disappear completely. In this situation the slow inward current can mediate action potentials (so called Ca action potentials). The slow inward current can be considered as the predominant mediator of the excitation process in the pacemaker cells of the sinoatrial node and the av node. Specific inhibitors of the slow membrane channel (verapamil, D 600, Ni, Co, and Mn ions) block the transmembrane Ca current leading to excitation contraction uncoupling. The excitation process will be impaired only if it is carried by the slow inward current alone. Specific inhibitors of the fast Na channel reduce the Na-dependent excitability of the myocardial cell without significant changes of the Ca current. The existence of 2 separate channels in the ventricular myocardium allows selective alteration of contractility without concomitant changes of the Na-dependent excitation process or, conversely, the reduction of excitability whereas the Ca current remains unchanged.