ARBs are used in patients who cannot take ACE inhibitors because they block which receptor?

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Multiple Choice

ARBs are used in patients who cannot take ACE inhibitors because they block which receptor?

Explanation:
ARBs block the angiotensin II receptor, specifically the AT1 receptor. Angiotensin II exerts its main effects—vasoconstriction and aldosterone release—through this receptor. By blocking AT1, ARBs prevent angiotensin II from binding, leading to vasodilation, less aldosterone-driven sodium and water retention, and lower blood pressure. This mechanism explains why ARBs are used when ACE inhibitors aren’t tolerated; they achieve similar downstream effects without increasing bradykinin, which is responsible for the cough and angioedema some patients experience with ACE inhibitors. The other options aren’t targets of ARBs: they don’t block dopamine, beta-adrenergic, or mineralocorticoid receptors.

ARBs block the angiotensin II receptor, specifically the AT1 receptor. Angiotensin II exerts its main effects—vasoconstriction and aldosterone release—through this receptor. By blocking AT1, ARBs prevent angiotensin II from binding, leading to vasodilation, less aldosterone-driven sodium and water retention, and lower blood pressure. This mechanism explains why ARBs are used when ACE inhibitors aren’t tolerated; they achieve similar downstream effects without increasing bradykinin, which is responsible for the cough and angioedema some patients experience with ACE inhibitors. The other options aren’t targets of ARBs: they don’t block dopamine, beta-adrenergic, or mineralocorticoid receptors.

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