Slow-channel depolarization: mechanism and control of arrhythmias

Abstract

The secondary inward current that flows through the slow channel is probably carried primarily by calcium ions. This current is responsible, in part, for the plateau phase of the cardiac action potential. Inward calcium current through the slow channel is essential to excitation-contraction coupling, and enhancement of this current exerts a positive inotropic effect. Transmembrane electrical potentials generated as a consequence of this slow inward current, so-called slow-channel depolarizations or slow responses, have been useful models in recent studies of cardiac autonomic interactions. The significance of the slow response in ventricular arrhythmias remains controversial and awaits more definitive experiments. The role of slow-channel depolarization as a basis for SA and AV nodal electrical activity is suggested by the electrophysiological similarities between these tissues and slow responses produced in vitro. This hypothesis is supported by the responses of these nodal tissues to interventions that augment of impede the slow inward current. More direct evidence in support of this notion may not be obtainable in the near future, since the critical voltage-clamp studies of ionic currents in SA and AV nodes are not technically feasible at this time.