Which mechanism primarily underlies the action of Milrinone?

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Milrinone functions primarily through the inhibition of phosphodiesterase III, an enzyme that breaks down cyclic adenosine monophosphate (cAMP). By inhibiting this enzyme, Milrinone increases the levels of cAMP within cardiac and smooth muscle cells. This increase in cAMP leads to enhanced myocardial contractility (positive inotropic effect) and vasodilation, which can improve cardiac output and decrease systemic vascular resistance. This mechanism is particularly useful in managing heart failure and acute decompensated heart failure, as it helps the heart to pump more efficiently while also addressing issues of vascular resistance.

The other options do not correctly describe the primary mechanism of Milrinone. Activation of alpha adrenoreceptors primarily causes vasoconstriction and increased blood pressure, which is not the main action of Milrinone. Inhibition of cGMP, which would typically lead to a decrease in vasodilation, does not align with the actions of Milrinone, as it works to enhance vasodilation through cAMP pathways. Lastly, stimulating the sympathetic nervous system (SNS) can lead to increased heart rate and contractility but is not the direct mechanism of action of Milrinone, which acts primarily through the inhibition of phosphodiester

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