What is the primary action of milrinone as an inotropic agent?

Milrinone acts primarily as a phosphodiesterase (PDE) inhibitor, specifically targeting phosphodiesterase type III. By inhibiting this enzyme, milrinone leads to increased levels of cyclic adenosine monophosphate (cAMP) within cardiac myocytes. Elevated cAMP levels enhance myocardial contractility, resulting in improved cardiac output. This mechanism makes milrinone an effective inotropic agent, particularly in the setting of heart failure.

Increased cAMP not only enhances the influx of calcium during the action potential but also promotes calcium release from the sarcoplasmic reticulum, contributing to stronger cardiac contractility. This dual effect is particularly beneficial in managing heart failure, as it supports the heart's ability to pump blood effectively.

The other choices presented involve different mechanisms or functions, such as modulation of sodium-potassium ATPase or interactions with beta receptors, which are not the primary actions attributed to milrinone. Thus, the increase in cAMP due to PDE inhibition is fundamentally what characterizes milrinone as an inotropic agent, underscoring its essential role in treating patients with compromised heart function.