Ionic basis of excitation mechanism in cardiac muscle.

Abstract

Cardiac electrical activity is due to passive ionic permeabilities and, partially, to nonneutral (electrogenic) active transport, but extracellular accumulation or depletion of potassium is also of importance. The rapid sodium current responsible for the spike of the action potential and the slow calcium or calcium and sodium inward current responsible for the plateau are governed by activation and inactivation variables, but the range of potential in which the corresponding conductances "open" or "close" differs markedly. For that reason, partially depolarized fibers exhibit slow action potentials deprived of a rapid ascending phase. The normal sinoatrial and atrioventricular node action potentials are of this type. Several components of of outward (repolarizing) currents, mainly carried by potassium ions (although anions may also carry repolarizing currents), exist, some of them being controlled by intracellular calcium. Repolarization is a much more labile process in Purkinje fibers than in myocardium. Recovery from inactivation of rapid and slow inward currents is important in controlling the shape of the action potential as a function of the previous diastole.