Vasopressin

Vasopressin, also called arginine vasopressin (AVP) or antidiuretic hormone (ADH), is a peptide hormone produced by neurons in the hypothalamus and released from the posterior pituitary gland. It is initially synthesized as a larger precursor that also includes neurophysin II and copeptin and is transported down axons to store in the neurohypophysis until released into the bloodstream.

In the kidney, AVP binds to V2 receptors on principal cells of the collecting ducts, promoting the insertion of aquaporin-2 water channels into the apical membrane and increasing water reabsorption. This action concentrates urine and reduces plasma osmolality. In vascular smooth muscle, AVP can activate V1a receptors, causing vasoconstriction at higher concentrations. V1b receptors, primarily in the anterior pituitary, influence adrenocorticotropic hormone release and the stress response.

Regulation of AVP secretion depends on osmoregulation and hemodynamic status. Hypothalamic osmoreceptors detect increases in plasma osmolality and trigger AVP release, while baroreceptors respond to changes in blood volume and pressure. Dehydration, hemorrhage, or stress can stimulate AVP secretion; excessive volume expansion or very low osmolality suppress it.

Clinically, AVP imbalance underlies several disorders. Central diabetes insipidus results from AVP deficiency, causing polyuria and polydipsia. Nephrogenic diabetes insipidus arises when kidneys are unresponsive to AVP. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) leads to excessive AVP activity and hyponatremia. Treatments include desmopressin, a V2-preferring analog used for central DI and some enuresis cases, and general fluid management for SIADH. Copeptin is studied as a stable biomarker for AVP activity. AVP analogs and antagonists have therapeutic roles in water balance disorders and in vasopressin-mediated hemodynamic management.