Anaes · Anaesthetic adjuncts

Vasopressin

Also known as Antidiuretic hormone (ADH) · Arginine vasopressin (AVP) · Non-adrenergic V1 peptide vasopressor · Catecholamine-sparing vasopressor

Vasopressin (antidiuretic hormone, ADH) is an endogenous PEPTIDE hormone released from the posterior pituitary that is fundamentally NOT a catecholamine — it acts through a completely separate, non-adrenergic receptor family. Its three receptors define its three actions: V1 (V1a) on vascular smooth muscle produces Gq-coupled vasoconstriction, V2 on the renal collecting duct produces Gs-coupled water reabsorption through aquaporin-2, and V3 (V1b) on the anterior pituitary drives ACTH release. As a vasopressor it works through V1 INDEPENDENT of adrenergic receptors, which is its defining advantage: it remains effective when adrenergic receptors are downregulated in septic shock and vasoplegia, the basis of its role as the catecholamine-sparing, catecholamine-resistant agent (Hiroto 2026, Dong 2026). The principal use is as a SECOND-LINE vasopressor in septic shock, added to noradrenaline when noradrenaline alone is insufficient — given at a FIXED dose of 0.03 to 0.04 units per min (NOT titrated to effect) and catecholamine-sparing, reducing the noradrenaline requirement (Hiroto 2026). Other uses are vasoplegia after cardiopulmonary bypass and — via its V2-selective synthetic analogue desmopressin (DDAVP) — central diabetes insipidus, haemophilia and von Willebrand disease (factor VIII and vWF release). It is given by IV infusion. The adverse-effect profile is the direct consequence of V1 vasoconstriction (peripheral, digital and MESENTERIC ISCHAEMIA) plus V2 water retention (HYPONATRAEMIA at high or prolonged doses), with decreased cardiac output from increased afterload and reflex bradycardia. Against noradrenaline, vasopressin is non-adrenergic (no tachyarrhythmia, effective when adrenergic receptors are downregulated) where noradrenaline is alpha-plus-beta-1 adrenergic — the two are used TOGETHER in septic shock. Against adrenaline the mechanism differs entirely (peptide versus catecholamine). Built on the septic-shock noradrenaline-and-vasopressin timing and dose study (Hiroto 2026), the neonatal fluid-refractory septic shock first-line vasopressor study (Yahya 2026), the vasopressor selection and postoperative delirium in older adults study (Dong 2026), and the carbon-monoxide-as-stress-axis-regulator study (Mancuso 2026).