Author + information
- ↵*Address for reprints: Arnold M. Katz, MD, Division of Cardiology, University of Connecticut, Farmington, Connecticut 06032
It is now generally agreed that Na+−K+adenosine triphosphatase (ATPase), a transport enzyme derived from the sarcolemmal sodium pump, is the primary site at which digitalis exerts its effects on the myocardial cell. Inhibition of the ability of this ion transport enzyme to catalyze Na+efflux from the cell in exchange for K+leads to both the therapeutic and toxic effects of the cardiac glycosides. The mechanism by which digitalis inhibits the sodium pump has been established in studies of Na+−K+ATPase which shpw that the ability of cardiac glycosides to inhibit adenosine triphosphate (ATP)-supported transport of Na+is reduced in the presence of elevated levels of K+. These studies explain the ability of hypokalemia to potentiate the effects of cardiac glycosides on the heart, and of high K+concentrations to overcome the inhibition of sodium pump activity by the cardiac glycosides. Recent demonstrations that the positive inotropic effect of the cardiac glycosides is correlated with an increased intracellular Na+provide strong evidence that these effects of digitalis to impair sodium efflux are responsible for the increased myocardial contractility caused by digitalis.
- American College of Cardiology Foundation