Vasopressin (arginine vasopressin, AVP) is an endogenous cyclic nonapeptide hormone (Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-Gly-NH2, MW ~1084.2 g/mol) synthesized in the hypothalamus and released from the posterior pituitary. It regulates water reabsorption in the renal collecting ducts via V2 receptors and mediates vasoconstriction via V1a receptors. Synthetic vasopressin (Vasostrict) is FDA-approved for vasodilatory shock and has been used for diabetes insipidus, esophageal variceal bleeding, and cardiac arrest.
Category: Reproductive / Hormonal. Evidence rating: A (strong human clinical data).
Clinical status: FDA-approved (Vasostrict for vasodilatory shock in adults)
Vasopressin acts on three receptor subtypes: V1a (vascular smooth muscle, hepatocytes), V1b/V3 (anterior pituitary corticotrophs), and V2 (renal collecting duct principal cells). V1a receptors are Gq-coupled; activation stimulates phospholipase C, increasing intracellular calcium and causing…
Safety considerations: Peripheral and splanchnic ischemia: digital ischemia, mesenteric ischemia, and skin necrosis reported with higher doses; Cardiac ischemia: coronary vasoconstriction may precipitate angina or myocardial infarction; Hyponatremia: excessive water retention via V2 receptor stimulation.
Reviewed by the PeptideAtlas Editorial Team. Last reviewed: 2026-07-06.
Related peptides: Kisspeptin, Gonadorelin, Oxytocin.
Compare: Vasopressin vs Kisspeptin, Vasopressin vs Gonadorelin, Vasopressin vs Oxytocin.
Vasopressin acts on V1a receptors to cause vasoconstriction through a catecholamine-independent mechanism, while norepinephrine acts on alpha-1 adrenergic receptors. In septic shock, vasopressin is often added to norepinephrine to provide a synergistic vasopressor effect and reduce catecholamine requirements.
Desmopressin has much greater V2 receptor selectivity and a longer half-life (approximately 2-4 hours vs 10-35 minutes for vasopressin), allowing convenient twice-daily or intranasal dosing. It also causes less V1a-mediated vasoconstriction.
Vasopressin is no longer a standalone recommendation in ACLS 2020 guidelines. While it may still be used as a vasopressor in cardiac arrest, epinephrine remains the primary recommended agent.