β-Adrenoceptor agonists increase membrane K⁺ conductance in cardiac Purkinje fibres

Abstract

Hormonal modulation of the ionic conductance of cell membranes is a topic of considerable current interest^1–3; it has a major role, for example, in the improved performance of the vertebrate heart elicited by sympathetic nerve stimulation or by circulating catecholamines, an effect involving enhanced calcium influx^3–6. β-Agonist catecholamines also abbreviate the action potential of cardiac Purkinje fibres^7–11, and increase the resting potential in a variety of cells^12–14, including cardiac cells^7,10,15–17, a hyperpolarization usually attributed to stimulation of the electrogenic Na⁺/K⁺ pump. We show here that nanomolar concentrations of β-catecholamines cause hyperpolarization of cardiac Purkinje fibres, not by increasing Na⁺/K⁺ pump current, but by increasing resting membrane K⁺ conductance. The hyperpolarization and shortening of the action potential should increase availability of Na⁺ channels and reduce the refractory period, effects tending to safeguard impulse propagation through the ventricular conducting system despite the increased heart rate caused by β-catecholamine action on the sinus node pacemaker.