How do angiotensin receptor blockers (ARBs) exert their effects?

Angiotensin receptor blockers (ARBs) primarily exert their effects by blocking the angiotensin II type 1 receptor. This receptor is crucial in mediating the physiological actions of angiotensin II, a potent vasoconstrictor that plays a significant role in regulating blood pressure and fluid balance.

When angiotensin II binds to the type 1 receptor, it causes vasoconstriction, increases blood pressure, stimulates aldosterone release from the adrenal glands (which leads to sodium and water retention), and promotes thirst. By blocking this receptor, ARBs inhibit these actions, leading to vasodilation, decreased blood pressure, reduced aldosterone secretion, and ultimately an increased excretion of sodium and water. This makes ARBs effective antihypertensive agents, used frequently in treating conditions like hypertension and heart failure.

Furthermore, ARBs do not increase bradykinin levels as angiotensin-converting enzyme (ACE) inhibitors do, nor do they promote aldosterone secretion; in fact, they generally reduce its secretion. Additionally, ARBs do not directly influence heart rate; their primary mechanism involves the modulation of blood pressure through their effects on the angiotensin II type 1 receptor.