Angiotensin II receptor type 1 (often discussed as "renin–angiotensin–aldosterone pathway" when describing the full pathway, but the specific molecular target is AT1R or AT2R) (AT1R (for Angiotensin II receptor type 1), AT2R (for Angiotensin II receptor type 2))

The Angiotensin II pathway comprises the production and action of angiotensin II, a potent peptide hormone involved in vasoconstriction, blood pressure regulation, and fluid/electrolyte homeostasis. Angiotensin II is produced from angiotensin I by ACE, then acts largely via AT1 and AT2 receptors, which are G protein-coupled receptors. AT1R mediates classical effects: vasoconstriction, sodium retention, aldosterone release, cellular proliferation, and increased blood pressure. AT2R plays a counter-regulatory, protective role, mediating vasodilation, anti-growth, anti-inflammation, and pro-apoptotic effects. Therapeutic intervention typically targets ACE or AT1R, as in hypertension and heart failure; AT2R is emerging as a novel target for anti-inflammatory and tissue-protective strategies. The pathway is central to many cardiovascular and renal diseases, and it is influenced by widely used therapeutic classes such as ACE inhibitors, ARBs, and direct renin inhibitors[1][2][4][5][6][7][8][9]. Note: The "Angiotensin II pathway" is not itself a canonical drug target; rather, its key molecular components (primarily AT1R, AT2R, and ACE/ACE2) are the true targets. The above information enables accurate mapping for database structuring and therapeutic decision-making.

Other names

Renin–angiotensin system (RAS)Renin–angiotensin–aldosterone system (RAAS)Angiotensin receptor pathwayAng II pathway

Blockade of the AT1R prevents vasoconstriction and aldosterone release (ARBs) - Inhibition of ACE reduces synthesis of Angiotensin II (ACE inhibitors) - Direct agonists (Angiotensin II) raise blood pressure via vasoconstriction and aldosterone stimulation - AT2R activation mediates vasodilation, anti-fibrotic, anti-inflammatory, and anti-proliferative effects