Angiotensin II type 1 receptor [1, 3] (AT1R [1])

The Angiotensin II type 1 receptor (AT1R) is a G protein-coupled receptor that serves as the primary mediator for the physiological actions of angiotensin II, the central effector peptide of the renin-angiotensin-aldosterone system (RAAS) [1, 3]. Upon activation, AT1R triggers potent vasoconstriction, stimulates the release of aldosterone from the adrenal cortex, and promotes renal sodium retention, all of which contribute to the regulation of blood pressure and fluid balance [2, 4]. Pathologically, overactivation of AT1R signaling is linked to hypertension, cardiac hypertrophy, and progressive renal damage [1, 2]. Pharmacological inhibition of this receptor using angiotensin II receptor blockers (ARBs) is a cornerstone of therapy for managing hypertension, heart failure, and diabetic nephropathy [2]. These drugs effectively lower blood pressure and provide organ protection by preventing the deleterious effects of angiotensin II-mediated signaling [2, 3].

Other names

AGTR1 [1, 3]AT1 [3]AT1R [2]Angiotensin II receptor type 1 [1]Type-1 angiotensin II receptor [3]

Angiotensin II receptor blockers (ARBs) selectively bind to the AT1 receptor, acting as competitive antagonists that block the binding of angiotensin II. This inhibition prevents the activation of downstream signaling pathways responsible for vasoconstriction, aldosterone release, and sympathetic nervous system activation, thereby lowering blood pressure and reducing target organ damage [2, 4].