5.5 - The Cardiac Action Potential

Abstract

This chapter examines the action potential as originating from sinoatrial (SA) nodal cells, atrial cells, or ventricular cells. The cardiac action potential takes a different form in different cardiac cells, including SA nodal cells, atrial muscle cells, atrioventricular nodal cells, Purkinje fibers, and ventricular muscle cells. The SA nodal cells have an unstable resting membrane potential that spontaneously depolarizes due to a pacemaker potential. This is caused by the funny Na+ current and a decrease in the conductance of the inward rectifier K+ channel. On reaching a threshold of about 255mV, an action potential begins by the progressive opening of T-type and L-type Ca2+ channels. The spike returns to baseline because of an increase in the delayed rectifier K+ current. The slope of the pacemaker potential and the resting membrane potential determine the time necessary to reach the threshold. Sympathetic stimulation increases the slope of the pacemaker potential and depolarizes the resting membrane potential. Both of these help increase the heart rate. Sympathetic stimulation releases norepinephrine that acts on the SA node through β1 receptors that are coupled to a Gs protein. Parasympathetic stimulation releases acetylcholine at terminals of the vagus nerve in the heart, which lowers the pacemaker potential and hyperpolarizes the cell. It is found that this reduces the frequency of action potentials originating at the SA node.