What is the mechanism of action of digoxin in heart failure?

Digoxin's mechanism of action in heart failure involves the inhibition of the Na+/K+ ATPase pump in cardiac myocytes. By blocking this pump, digoxin leads to an increase in intracellular sodium levels. As sodium levels rise, the sodium-calcium exchanger, which normally extrudes calcium from the cell in exchange for sodium, is inhibited. This results in increased intracellular calcium concentrations, which enhances the force of cardiac contraction (positive inotropic effect). The increased calcium availability also contributes to improved myocardial contractility, making it particularly effective in treating heart failure, where the heart's pumping ability is compromised.

The other options do not accurately represent digoxin's mechanism of action. Blocking beta-adrenergic receptors, as described in one of the options, is characteristic of beta-blockers, which can also be used in heart failure but work through a different pathway. The inhibition of phosphodiesterase, which increases cAMP levels, is primarily associated with drugs like milrinone, a phosphodiesterase inhibitor, rather than digoxin. Meanwhile, increasing nitric oxide production to promote vasodilation is a mechanism associated with drugs like nitrates, and not with digoxin, which primarily focuses on contractility rather than vascular effects.