Milrinone MOA involves which mechanism?

Milrinone MOA involves which mechanism?

• A. PDE-3 inhibition leading to increased cAMP
• B. Beta-adrenergic receptor blockade
• C. Calcium chelation
• D. ACE inhibition

Answer: (A)

Milrinone’s main mechanism is inhibition of phosphodiesterase-3, which normally breaks down cyclic AMP in cardiac and vascular smooth muscle. By blocking PDE-3, milrinone raises intracellular cAMP, activating protein kinase A. In heart cells, this increases calcium entry and release, boosting contractility (positive inotropy). In vascular smooth muscle, higher cAMP reduces calcium sensitivity and promotes relaxation, causing vasodilation and lower afterload. This dual inotropic and vasodilatory effect explains its use as an inodilator in acute heart failure. The other options don’t fit: beta-blockade would decrease cAMP and contractility, calcium chelation would reduce calcium directly, and ACE inhibition lowers angiotensin II without raising cAMP.

Milrinone’s main mechanism is inhibition of phosphodiesterase-3, which normally breaks down cyclic AMP in cardiac and vascular smooth muscle. By blocking PDE-3, milrinone raises intracellular cAMP, activating protein kinase A. In heart cells, this increases calcium entry and release, boosting contractility (positive inotropy). In vascular smooth muscle, higher cAMP reduces calcium sensitivity and promotes relaxation, causing vasodilation and lower afterload. This dual inotropic and vasodilatory effect explains its use as an inodilator in acute heart failure. The other options don’t fit: beta-blockade would decrease cAMP and contractility, calcium chelation would reduce calcium directly, and ACE inhibition lowers angiotensin II without raising cAMP.