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approvedHormone Regulation

Vasopressin

Also known as: ADH, Antidiuretic Hormone, AVP, Arginine Vasopressin, Pitressin, Vasostrict

Vasopressin (arginine vasopressin/ADH) is an endogenous nonapeptide hormone produced in the hypothalamus and released from the posterior pituitary that regulates water balance, blood pressure, and social behavior. Synthetically manufactured as Vasostrict, it is FDA-approved for the treatment of vasodilatory shock (including septic shock) and diabetes insipidus. It acts through three receptor subtypes — V1a (vasoconstriction), V1b (ACTH release), and V2 (antidiuresis) — making it a critical rescue agent in hypotension refractory to catecholamines and a first-line pressor in certain cardiac arrest protocols.

3 cited references·5 researched benefits

Quick Answer

Vasopressin (ADH) is an endogenous nonapeptide hormone that regulates water balance and blood pressure through V1a (vasoconstriction), V1b (ACTH release), and V2 (antidiuresis) receptors. FDA-approved as Vasostrict for vasodilatory shock and diabetes insipidus, it is a critical ICU medication used when catecholamine pressors are insufficient. In cardiac arrest, vasopressin is included in ACLS protocols as an alternative to epinephrine.

Key Facts

Mechanism
Vasopressin activates three receptor subtypes with distinct physiological effects. V1a receptors on vascular smooth muscle trigger Gq-mediated phospholipase C activation, IP3/DAG signaling, and intracellular calcium release, causing potent vasoconstriction in splanchnic, renal, and cutaneous vascular beds. This is independent of adrenergic signaling, explaining vasopressin's effectiveness in catecholamine-resistant shock where adrenergic receptors may be downregulated. V1b receptors on anterior pituitary corticotrophs stimulate ACTH secretion. V2 receptors on renal collecting duct principal cells activate the Gs/cAMP/PKA cascade that drives aquaporin-2 translocation to the apical membrane, increasing water reabsorption and producing concentrated urine. In septic shock, relative vasopressin deficiency (depletion of pituitary stores) contributes to refractory hypotension, providing the rationale for exogenous replacement.
Research Status
approved
Half-Life
~10-20 minutes (plasma)
Molecular Formula
C₄₆H₆₅N₁₅O₁₂S₂
Primary Use
Hormone Regulation
Table of Contents

Benefits

  • Raises blood pressure in vasodilatory shock — effective through non-adrenergic mechanism when catecholamine pressors fail or cause excessive tachycardiastrong
  • Treats central diabetes insipidus — replaces deficient ADH, correcting polyuria and polydipsiastrong
  • Included in ACLS cardiac arrest protocols — may be used as alternative or adjunct to epinephrine in pulseless arreststrong
  • Reduces catecholamine requirements in septic shock — the VASST trial showed vasopressin spares norepinephrine dosing and may improve outcomes in less severe septic shockstrong
  • Controls variceal and GI hemorrhage — splanchnic vasoconstriction reduces portal pressure and bleeding from esophageal varicesmoderate

Dosage Protocols

RouteDosage RangeFrequencyNotes
Intravenous infusion (vasodilatory shock)0.01-0.04 units/minContinuous infusion, titrated to MAPVasostrict standard dosing. Doses >0.04 units/min associated with increased ischemic complications without additional hemodynamic benefit. Used as adjunct to norepinephrine in septic shock per Surviving Sepsis guidelines.
Intravenous bolus (cardiac arrest, ACLS)40 unitsSingle dose, may replace first or second dose of epinephrineUsed in pulseless VT/VF and PEA/asystole. Current AHA guidelines have de-emphasized vasopressin in favor of epinephrine alone, though it remains an acceptable alternative.
Intravenous infusion (GI hemorrhage)0.2-0.4 units/minContinuous infusion for up to 24-72 hoursUsed for variceal bleeding when endoscopic therapy is not immediately available. Often co-administered with nitroglycerin to counteract coronary vasoconstriction. Largely replaced by octreotide/terlipressin in current practice.
Intramuscular/subcutaneous (diabetes insipidus)5-10 unitsEvery 4-6 hours as neededAqueous vasopressin (Pitressin) for acute DI management. Short duration of action makes it less convenient than desmopressin for chronic use but useful in post-surgical or ICU settings.

Medical disclaimer

Dosage information is provided for educational reference only. Always follow your prescriber's instructions and consult a qualified healthcare provider before starting any peptide protocol.

Side Effects

  • Digital, mesenteric, and coronary ischemia — potent vasoconstriction can cause tissue ischemia, gangrene of extremities, and myocardial ischemia at high dosesserious
  • Hyponatremia — excessive water retention through V2 receptor activation, particularly with higher doses or when combined with free water administrationserious
  • Arrhythmias — bradycardia, atrial fibrillation, and other conduction disturbances due to coronary vasoconstriction and baroreceptor-mediated reflexserious
  • Abdominal cramping and nausea — due to smooth muscle contraction in the GI tract, occurring in 10-20% of patientscommon
  • Skin necrosis at injection/infusion sites — extravasation can cause severe tissue damage; must be administered through central venous access when possibleserious

Frequently Asked Questions

Why is vasopressin used in septic shock when norepinephrine is already being given?
In septic shock, massive vasodilation and inflammatory downregulation of adrenergic receptors can make patients resistant to catecholamines like norepinephrine. Vasopressin works through an entirely different mechanism (V1a receptors, not adrenergic receptors) and exploits the fact that sepsis depletes endogenous vasopressin stores. The VASST trial showed that adding low-dose vasopressin (0.03 units/min) to norepinephrine was safe and reduced total norepinephrine requirements. Current Surviving Sepsis Campaign guidelines recommend adding vasopressin (up to 0.03 units/min) when norepinephrine alone is insufficient to achieve target MAP of 65 mmHg.
What is the difference between vasopressin and desmopressin?
Vasopressin activates all three receptor subtypes — V1a (vasoconstriction), V1b (ACTH release), and V2 (antidiuresis). Desmopressin is a modified synthetic analog that is highly selective for V2 receptors, providing potent antidiuretic effects without significant vasoconstriction. Vasopressin has a half-life of 10-20 minutes; desmopressin lasts 2-3 hours. Vasopressin is used in critical care for shock and cardiac arrest (where vasoconstriction is desired), while desmopressin is used for diabetes insipidus, bedwetting, and bleeding disorders (where antidiuresis and vWF release are desired without cardiovascular effects).
Is vasopressin still recommended in cardiac arrest?
The role of vasopressin in cardiac arrest has evolved. The 2010 AHA guidelines included 40 units IV vasopressin as an alternative to the first or second dose of epinephrine. However, the 2015 and subsequent guidelines removed vasopressin as a recommended agent, based on evidence (including the VAM and other trials) showing no clear survival benefit over epinephrine alone. Vasopressin remains an acceptable option but is no longer specifically recommended. The emphasis has shifted to high-quality CPR, early defibrillation, and epinephrine as the primary vasoactive agent.
Why does vasopressin cause digital ischemia and gangrene?
Vasopressin causes potent V1a-mediated vasoconstriction in peripheral vascular beds, including the digital arteries of fingers and toes. At higher doses (>0.04 units/min), sustained constriction of these end-arteries reduces blood flow below the threshold for tissue viability, causing ischemia that can progress to gangrene if the infusion is not reduced. Risk factors include pre-existing peripheral vascular disease, high vasopressin doses, and concurrent high-dose catecholamines. This is why doses above 0.04 units/min are generally avoided and why monitoring for skin mottling, cyanosis, and digital pallor is essential during infusion.

References

  1. 1
    Vasopressin versus norepinephrine infusion in patients with septic shock (VASST trial)(2003)PubMed ↗
  2. 2
    Vasopressin in hemorrhagic shock: a systematic review and meta-analysis(2013)PubMed ↗
  3. 3
    Vasopressin and its analogues: from natural hormones to multitasking peptides(2007)PubMed ↗

Latest Research

Last updated: 2026-02-19