Arginine vasopressin receptor (AVPR) (AVPR)

The Arginine vasopressin receptor (AVPR) family, consisting of the V1a, V1b, and V2 subtypes, are G protein-coupled receptors that mediate the physiological actions of the neurohypophyseal hormone arginine vasopressin (AVP) [4, 9, 19]. AVP is synthesized from the AVP gene as a large precursor molecule, pro-vasopressin (or prepro-vasopressin), which is cleaved during axonal transport into active AVP, neurophysin II, and the C-terminal fragment known as copeptin [3, 5, 11]. The V2 receptor subtype is primarily responsible for regulating water reabsorption in the renal collecting ducts via aquaporin-2 channels, whereas V1a and V1b receptors mediate vasoconstriction and the neuroendocrine stress response, respectively [2, 13, 18, 19]. Dysregulation of the vasopressin system is central to several clinical conditions, including diabetes insipidus, the syndrome of inappropriate antidiuretic hormone secretion (SIADH), and congestive heart failure [1, 7, 12]. Therapeutic strategies involve the use of agonists such as desmopressin for hormone replacement in diabetes insipidus and antagonists known as vaptans to manage hyponatremia and fluid overload [16, 17, 18]. Additionally, the stable precursor fragment copeptin serves as a robust clinical biomarker for assessing AVP release and hemodynamic stress [1, 8, 11].

Other names

Prepro-arginine-vasopressin-neurophysin IIArginine vasopressinAVPAntidiuretic hormone receptorVasopressin V1a receptorVasopressin V1b receptorVasopressin V2 receptorCopeptinCT-proAVPAVPR1AAVPR1BAVPR2

Drugs act as either agonists or antagonists at specific Arginine vasopressin receptor subtypes. V2 receptor agonists stimulate the Gs protein-adenylyl cyclase pathway to increase cAMP, leading to the insertion of aquaporin-2 channels into the renal collecting duct for water reabsorption [16, 19, 21]. V2 receptor antagonists (vaptans) block this effect to promote aquaresis (solute-free water excretion) [16, 17]. V1a and V1b receptor activation stimulates the Gq/11 protein and phospholipase C pathway, increasing intracellular calcium to induce vasoconstriction and the release of adrenocorticotropic hormone (ACTH) [13, 18, 19].