What is the mechanism of action for angiotensin-converting enzyme (ACE) inhibitors?

Angiotensin-converting enzyme (ACE) inhibitors work primarily by inhibiting the conversion of angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor that plays a key role in regulating blood pressure and fluid balance in the body. By blocking this conversion, ACE inhibitors lead to decreased levels of angiotensin II, resulting in vasodilation, reduced blood pressure, and decreased aldosterone secretion. This promotes natriuresis (excretion of sodium in urine) and diuresis (increased urine production), helping to alleviate conditions such as hypertension and heart failure.

In contrast, other options focus on different mechanisms that do not relate to how ACE inhibitors function. For instance, the blockade of calcium channels pertains to calcium channel blockers, which operate by inhibiting calcium influx into cells affecting vascular smooth muscle contraction. Promoting sodium and water retention is contrary to the effects of ACE inhibitors, as they lead to natriuresis and decreased fluid retention. Lastly, the inhibition of beta-adrenergic receptors is specific to beta-blockers, which primarily affect heart rate and myocardial contractility, rather than directly influencing the renin-angiotensin-aldosterone system. This highlights the unique role of