Vasopressin V1 receptor and Vasopressin V2 receptor (V1 receptor (V1R, AVPR1A), V2 receptor (V2R, AVPR2))

Vasopressin receptors are a family of G protein-coupled receptors that mediate the actions of the neurohypophyseal hormone vasopressin. There are three main subtypes relevant in human physiology: V1A (mainly called V1), V1B (historically V3), and V2. The V1 receptor (AVPR1A) is primarily expressed in vascular smooth muscle, liver, platelets, and brain, and mediates vasoconstriction, myocardial hypertrophy, and platelet aggregation through Gq protein–mediated activation of phospholipase C and increased intracellular calcium. The V2 receptor (AVPR2) is expressed in the renal collecting duct and vascular endothelium, controlling antidiuretic effects by stimulating aquaporin-2 insertion for water reabsorption via Gs-coupled activation of adenylyl cyclase and cAMP. Mutations in V2 are a major cause of nephrogenic diabetes insipidus. V1B (AVPR1B) is found in the anterior pituitary and regulates release of ACTH and other hormones. Vasopressin receptor subtypes are established therapeutic targets in disorders of water balance, shock, and select endocrine or coagulation disorders, and are targeted by both agonist and antagonist drugs[1][2][3][4][5][6][7].

Other names

V1a receptor (for AVPR1A)V1b receptor (for AVPR1B; sometimes called V3 receptor)V2 receptor (for AVPR2)Arginine vasopressin receptor 1A, 1B, 2AVPR1AAVPR1BAVPR2

Agonists (e.g., vasopressin, desmopressin) activate V1 and/or V2 receptors to produce vasoconstriction or antidiuresis Antagonists (e.g., vaptans) block V2 receptor–mediated water reabsorption, producing aquaresis V1 antagonists inhibit vasoconstriction and platelet aggregation Some drugs act as selective/non-selective antagonists on V1A, V1B, or V2 subtypes