Angiotensin II type 1 receptor (AT1R) (AT1R)

The Angiotensin II type 1 receptor (AT1R) is a critical G protein-coupled receptor that mediates the primary physiological effects of angiotensin II, the main effector peptide of the renin-angiotensin system (RAS) [1, 4]. Upon activation, AT1R triggers potent vasoconstriction, stimulates aldosterone release from the adrenal cortex, and promotes renal sodium reabsorption, all of which contribute to the elevation of systemic blood pressure [1, 2]. Pathologically, overactivation of AT1R is a central driver in the development of hypertension, congestive heart failure, and progressive renal damage [2, 4]. Therapeutic intervention typically involves the use of angiotensin II receptor blockers (ARBs), such as olmesartan, which selectively bind to and inhibit the receptor [3]. These drugs are widely utilized to manage cardiovascular and renal diseases by reducing peripheral vascular resistance and protecting end-organ function [2, 3]. Understanding the structural dynamics of AT1R-drug interactions remains vital for optimizing treatment efficacy and minimizing adverse effects like hyperkalemia or renal dysfunction [2].

Other names

AGTR1Angiotensin II receptor type 1AT1 receptorAT1

Competitive antagonism of the angiotensin II type 1 receptor, preventing the binding of angiotensin II and thereby inhibiting its vasopressor and aldosterone-secreting effects [2, 3].