What is the mechanism of action of ACE inhibitors in hypertension?

What is the mechanism of action of ACE inhibitors in hypertension?

• A. Block calcium channels in vascular smooth muscle
• B. Inhibit angiotensin-converting enzyme, preventing angiotensin II formation
• C. Block beta-adrenergic receptors in the heart
• D. Enhance production of nitric oxide in blood vessels

Answer: (B)

ACE inhibitors play a crucial role in managing hypertension by targeting the renin-angiotensin-aldosterone system (RAAS). The primary mechanism of action for ACE inhibitors is the inhibition of angiotensin-converting enzyme (ACE). By inhibiting this enzyme, ACE inhibitors effectively reduce the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. This leads to a decrease in vasoconstriction and a subsequent reduction in blood pressure. Additionally, the reduction of angiotensin II levels leads to decreased secretion of aldosterone, which normally promotes sodium and water retention. This effect further contributes to the lowering of blood pressure by reducing blood volume. Therefore, the overall effect of ACE inhibitors is a reduction in systemic vascular resistance and a decrease in cardiac output, making them effective antihypertensive agents.

ACE inhibitors play a crucial role in managing hypertension by targeting the renin-angiotensin-aldosterone system (RAAS). The primary mechanism of action for ACE inhibitors is the inhibition of angiotensin-converting enzyme (ACE). By inhibiting this enzyme, ACE inhibitors effectively reduce the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. This leads to a decrease in vasoconstriction and a subsequent reduction in blood pressure.

Additionally, the reduction of angiotensin II levels leads to decreased secretion of aldosterone, which normally promotes sodium and water retention. This effect further contributes to the lowering of blood pressure by reducing blood volume. Therefore, the overall effect of ACE inhibitors is a reduction in systemic vascular resistance and a decrease in cardiac output, making them effective antihypertensive agents.