Vasopressin
The endogenous nine-amino-acid posterior-pituitary hormone that regulates water balance, vascular tone, and the stress axis — FDA-approved for central diabetes insipidus and vasodilatory shock.
What is Vasopressin?
Arginine vasopressin (AVP), also called antidiuretic hormone (ADH), is a nine-amino-acid cyclic nonapeptide (Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-Gly-NH2, closed by a disulfide bridge between the two cysteines) synthesized in magnocellular and parvocellular neurons of the hypothalamic supraoptic and paraventricular nuclei and released from the posterior pituitary. It is the body's master regulator of water conservation and a backup pressor hormone deployed when blood pressure falls. Vasopressin acts at three G-protein-coupled receptors: V2 in the renal collecting duct (water reabsorption via aquaporin-2 insertion), V1a on vascular smooth muscle (vasoconstriction), and V1b on anterior pituitary corticotrophs (ACTH release). Synthetic vasopressin is FDA-approved as Pitressin for central diabetes insipidus and, in the ICU, for vasodilatory/septic shock. The V2-selective analogue desmopressin and the V1-selective analogue terlipressin are derivatives built from the native sequence.
What Vasopressin Is Investigated For
Native vasopressin is, unusually for a peptide on this site, a drug that lives almost entirely inside the hospital. The two settled indications are central diabetes insipidus (where it replaces the missing endogenous hormone) and vasodilatory shock — most often septic shock — where a low-dose fixed infusion (typically 0.03 U/min) is added to norepinephrine to reduce catecholamine exposure. The VASST trial (Russell et al., 2008) did not show overall 28-day mortality benefit but did support safety and a possible signal in less-severe shock, and subsequent individual-patient-data meta-analysis found no effect on mortality but reduced renal replacement therapy requirements. Current Surviving Sepsis Campaign guidance recommends adding vasopressin to norepinephrine when MAP is inadequate rather than escalating norepinephrine monotherapy. Post-cardiac-surgery vasoplegia, hepatorenal syndrome (via the V1-selective analogue terlipressin), and cardiac arrest use are supporting rather than headline roles. The copeptin assay — measuring a cleaved byproduct of AVP — has largely replaced direct AVP measurement as the laboratory surrogate for endogenous vasopressin activity in endocrine workups. Outside these clinical niches, vasopressin is not a wellness or self-administered peptide — its nonselective V1a activity makes chronic self-use dangerous in a way desmopressin's V2 selectivity does not.
History & Discovery
The clinical story of vasopressin begins in 1895, when George Oliver and Edward Schäfer demonstrated that extracts of the posterior pituitary gland raised blood pressure when injected into dogs — the first pharmacological evidence for what would later be called vasopressin. By the 1910s, Henry Dale had characterized the uterotonic and antidiuretic activities of posterior pituitary extracts, and from the 1920s forward such extracts (under names like Pitressin and Pituitrin) were used clinically for diabetes insipidus, postpartum hemorrhage, and shock — crude preparations containing a mix of what we now know as vasopressin and oxytocin. The structural characterization and synthesis of vasopressin were achieved by Vincent du Vigneaud and colleagues at Cornell University Medical College in the early 1950s, building directly on their 1953 synthesis of oxytocin — the first laboratory synthesis of any polypeptide hormone. Du Vigneaud's group identified vasopressin as a cyclic nonapeptide closed by a disulfide bridge between two cysteines, differing from oxytocin at only two positions (phenylalanine vs. isoleucine at position 3; arginine vs. leucine at position 8). He was awarded the 1955 Nobel Prize in Chemistry for this work, which established peptide-hormone chemistry as a tractable discipline. The fact that two hormones with such different physiology — water balance and vasoconstriction vs. uterine contraction and milk ejection — could differ by just two amino acids became one of the earliest and most striking illustrations of structure-function specificity at a receptor level. The clinical pharmacology of vasopressin matured alongside that chemistry. Ferring Pharmaceuticals developed desmopressin (1-deamino-8-D-arginine vasopressin) in the 1960s by deaminating position 1 and substituting D-arginine for L-arginine at position 8, which virtually eliminated V1a pressor activity while preserving V2 antidiuretic activity — the analogue now used for ambulatory diabetes insipidus, bedwetting, and hemostatic indications. Terlipressin (triglycyl-lysine vasopressin), a V1-selective prodrug, was developed in Europe in the 1970s and 1980s for variceal bleeding and hepatorenal syndrome and received FDA approval as Terlivaz for hepatorenal syndrome in 2022 on the basis of the CONFIRM trial. The modern era of native vasopressin in critical care dates to the late 1990s and early 2000s. Landry and Oliver's 2001 NEJM review articulated the relative-vasopressin-deficiency hypothesis in late septic shock — endogenous AVP stores are initially mobilized by baroreflex activation but become depleted after hours to days of sustained shock, removing a physiologic backstop against vasodilation. This provided the rationale for low-dose exogenous vasopressin infusion as a catecholamine-sparing adjunct, which was tested in the VASST trial (Russell et al., NEJM 2008) and the VANISH trial (Gordon et al., JAMA 2016). Neither trial showed a mortality benefit, but vasopressin earned a durable role in ICU vasopressor algorithms and current Surviving Sepsis Campaign guidance.
How It Works
Vasopressin is the hormone your body releases when it needs to hold onto water or prop up blood pressure. It tells the kidneys to reabsorb water (making urine more concentrated) and tells blood vessels to tighten. In the ICU, a synthetic version is infused to support blood pressure in septic shock when norepinephrine alone isn't enough.
Vasopressin exerts its effects through three distinct G-protein-coupled receptors. The V2 receptor, coupled to Gs and the cAMP/PKA cascade, is expressed on the basolateral membrane of renal collecting-duct principal cells; activation drives trafficking of aquaporin-2 water channels to the apical membrane, increasing water reabsorption and concentrating urine. The V1a receptor, coupled to Gq and the PLC/IP3/DAG cascade, is expressed on vascular smooth muscle and mediates vasoconstriction — the clinical 'pressor' effect — and also contributes to platelet aggregation and hepatic glycogenolysis. The V1b (also called V3) receptor, also Gq-coupled, is expressed on anterior pituitary corticotrophs and drives ACTH release as part of the stress axis, particularly during sustained or chronic stress. Endogenous release is controlled by two principal stimuli: plasma osmolality (detected by hypothalamic osmoreceptors, the dominant physiological driver under normal conditions) and effective circulating volume or arterial pressure (detected by cardiopulmonary and arterial baroreceptors, a higher-threshold but more powerful stimulus). A plasma osmolality rise of about 1% produces measurable AVP release and antidiuresis; a blood pressure drop of more than 10-20% produces dramatic, high-amplitude AVP release that can reach pressor concentrations. This dual regulation explains why septic shock — where peripheral vasodilation causes functional hypovolemia — initially provokes high endogenous AVP release that is then paradoxically depleted over hours to days, producing a relative vasopressin deficiency that underpins the therapeutic rationale for exogenous vasopressin infusion. Structurally, vasopressin is a close cousin of oxytocin: both are nine-amino-acid cyclic peptides cleaved from related precursors in adjacent hypothalamic neurons, differing only at positions 3 (phenylalanine in vasopressin, isoleucine in oxytocin) and 8 (arginine vs. leucine). The shared neurohypophysial lineage and near-identical backbone explain their cross-reactivity at each other's receptors and their co-evolution across vertebrate phylogeny.
Evidence Snapshot
Human Clinical Evidence
Extensive. Vasopressin's physiology is one of the most thoroughly studied hormonal systems, and clinical use in diabetes insipidus and vasodilatory shock is backed by landmark RCTs (VASST 2008, VANISH 2016), individual-patient-data meta-analyses, and current Surviving Sepsis Campaign guidelines.
Animal / Preclinical
Comprehensive. AVP receptor pharmacology, osmoregulation, baroreflex, and HPA-axis interactions are characterized across multiple species.
Mechanistic Rationale
Very strong. V1a, V1b, and V2 receptor signaling pathways are well-mapped, and the relative-deficiency rationale for AVP in septic shock is grounded in serial human hormone measurements.
Research Gaps & Open Questions
What the current literature has not yet settled about Vasopressin:
- 01Optimal timing of vasopressin initiation in septic shock — whether to start at low norepinephrine doses (early) or reserve for refractory shock (late) is not resolved by current trial evidence, and the VANISH trial's early-initiation approach did not show mortality benefit.
- 02Identification of vasopressin responder subgroups — the VASST signal for benefit in less-severe shock and the reduction in RRT requirement across meta-analyses suggest heterogeneity of treatment effect that is not yet well characterized by clinical or biomarker features.
- 03Dose ceiling and upward titration — whether modestly higher infusion rates (up to 0.067 U/min) are safe and beneficial in refractory shock remains controversial, with most guidelines capping at 0.03-0.04 U/min to limit ischemic risk.
- 04Role of copeptin as a real-time shock biomarker — copeptin is an established diagnostic tool for AVP deficiency, but its utility to guide vasopressin dosing or predict response in shock patients is only beginning to be studied.
- 05V1a-selective and V1a/V2 dual agonists for specific shock phenotypes — terlipressin has an established hepatorenal syndrome role, but its positioning vs. native vasopressin in septic shock is still being defined.
- 06Long-term neurocognitive and social effects of exogenous vasopressin exposure — the animal literature on V1a central effects (social behavior, aggression, bonding) has not translated into well-characterized human outcomes after ICU vasopressin exposure.
- 07Pediatric vasopressin use in shock — most trial evidence is adult, and optimal dosing, indication selection, and outcomes in pediatric septic shock are less well defined.
Forms & Administration
In clinical practice, native vasopressin is administered as an IV continuous infusion (typical septic-shock dose 0.03 units/min, with acceptable range 0.01-0.04 U/min) or as intermittent IM/subQ injection (5-10 units every 3-4 hours for central diabetes insipidus in the inpatient setting, when desmopressin is unavailable). It is a hospital- and ICU-restricted medication requiring continuous hemodynamic monitoring. Native vasopressin is not meaningfully absorbed orally and is degraded rapidly in plasma (half-life 10-20 minutes), which is why ambulatory antidiuretic replacement uses the long-acting, V2-selective analogue desmopressin rather than native AVP. All vasopressin-class peptides should only be administered under the guidance of a qualified healthcare provider. Never self-administer without clinician oversight.
Dosing & Protocols
The ranges below reflect protocols commonly discussed in the literature and by clinicians — not a prescription. Actual dosing for any individual should be determined by a qualified healthcare provider who knows the patient.
Typical Range
Septic and vasodilatory shock (ICU, as adjunct to norepinephrine): continuous IV infusion starting at 0.03 units/min, typically titrated within 0.01-0.04 U/min; doses above 0.04 U/min are generally avoided due to rising ischemic risk. Central diabetes insipidus (inpatient, when desmopressin is unavailable): 5-10 units IM or subQ every 3-4 hours as needed, or continuous IV infusion at 0.5-10 milliunits/kg/hour titrated to urine output and serum sodium. Post-cardiopulmonary-bypass vasoplegia: similar infusion rates to septic shock, with protocols varying by institution. Cardiac arrest (historical, now largely replaced by epinephrine-only protocols in most guidelines): 40-unit IV bolus replacing or following epinephrine.
Frequency
In shock, vasopressin is given as a continuous IV infusion through a central line with continuous blood pressure monitoring, not as bolus dosing (bolus doses can produce excessive transient vasoconstriction). In diabetes insipidus, intermittent IM/subQ dosing is scheduled to anticipate polyuria breakthrough rather than following a fixed pulse pattern. No outpatient self-administration is appropriate.
Timing Considerations
No specific timing requirements: can be administered at any time of day, with or without food, and is not tied to exercise timing. Consistency matters more than the specific clock — dose at roughly the same time each day (or same day each week, for weekly protocols) to keep exposure steady.
Cycle Length
Shock infusions continue until the patient is weaned from catecholamine support or until goals of care change; typical durations range from hours to several days. Diabetes insipidus use is as a bridge to oral or intranasal desmopressin once the patient is stable enough for ambulatory management. No chronic ambulatory use of native vasopressin is standard of care; desmopressin fills that role.
Protocol Notes
Vasopressin in vasodilatory shock is fundamentally a catecholamine-sparing strategy rather than a stand-alone pressor. Current Surviving Sepsis Campaign guidance is to add vasopressin at 0.03 U/min when norepinephrine doses above roughly 0.25-0.5 mcg/kg/min are insufficient to maintain mean arterial pressure, rather than escalating norepinephrine further. The rationale is twofold: vasopressin acts through a non-catecholamine pathway (V1a-Gq) so it is not subject to adrenergic receptor desensitization, and it appears to correct the relative AVP deficiency that develops in late shock. Dose escalation above 0.04 U/min is controversial — higher doses (up to 0.067 U/min in some reports) may further raise blood pressure but at meaningfully increased risk of digital, mesenteric, and coronary ischemia. Extravasation from a peripheral line can cause local tissue necrosis; central venous administration is strongly preferred. Weaning protocols vary: some units discontinue vasopressin first and continue norepinephrine; others do the reverse. The evidence base does not clearly favor one approach. For central diabetes insipidus, native aqueous vasopressin has largely been supplanted by desmopressin for both inpatient and outpatient management. The main residual role for native vasopressin in DI is in hemodynamically unstable patients where precise titration to urine output and serum sodium is required, or in institutions where desmopressin formulations are temporarily unavailable. The copeptin assay — a sandwich immunoassay measuring the C-terminal glycopeptide cleaved from pre-pro-AVP — is now the preferred laboratory surrogate for endogenous AVP release, since AVP itself is unstable in plasma and binds to platelets. Copeptin rises in parallel with AVP and is used diagnostically in polyuria-polydipsia workups (hypertonic saline or arginine stimulation), hyponatremia evaluation, and as a prognostic biomarker in sepsis and myocardial infarction.
Native vasopressin is a hospital- and ICU-restricted medication. It should not be used outside a monitored setting. Self-administration is not appropriate for any indication; ambulatory vasopressin-pathway replacement uses the V2-selective analogue desmopressin.
Timeline of Effects
Onset
IV vasopressin produces measurable pressor effect within minutes of infusion initiation — V1a-mediated vasoconstriction is nearly immediate, with mean arterial pressure typically rising within 5-15 minutes of reaching the target infusion rate. Renal antidiuretic effect from a single IM/subQ dose in diabetes insipidus is apparent within 30-60 minutes, with urine output falling and urine osmolality rising. ACTH release via V1b receptors is similarly rapid in response to endogenous vasopressin release or exogenous infusion.
Peak Effect
Peak pressor effect in a continuous infusion is reached within 30-60 minutes of dose stabilization, with blood pressure effects plateauing so long as the infusion rate is held constant. Antidiuretic effect from a single dose peaks at 1-2 hours and persists for 3-6 hours, depending on route. Plasma half-life is short — approximately 10-20 minutes for circulating native AVP — which is why continuous infusion rather than intermittent dosing is used for shock.
After Discontinuation
Hemodynamic effects dissipate within 30-60 minutes of stopping a continuous infusion, sometimes producing rebound hypotension that must be managed with norepinephrine titration. Antidiuretic effect from the last IM/subQ dose is gone within 6-8 hours, and untreated diabetes insipidus will reemerge as polyuria. There is no physical dependence or withdrawal syndrome in the usual sense — the drug simply wears off and the underlying disorder reasserts itself.
Common Questions
Who Vasopressin Is NOT For
- •Known hypersensitivity to vasopressin, chlorobutanol (present in some formulations), or other formulation excipients.
- •Chronic nephritis with nitrogen retention — antidiuretic response is unreliable and fluid overload risk is high.
- •Coronary artery disease with unstable angina or recent myocardial infarction — V1a-mediated coronary vasoconstriction can precipitate ischemia; benefit-risk must be weighed individually in the ICU setting.
- •Severe peripheral vascular disease or Raynaud's phenomenon — risk of digital ischemia and necrosis is meaningfully elevated at therapeutic pressor doses.
- •Mesenteric ischemia or documented mesenteric vascular disease — V1a vasoconstriction of splanchnic vasculature can extend infarction.
- •Hypersensitivity to beef- or pork-derived peptides in the case of older extract-based preparations (almost entirely historical; modern formulations are synthetic).
- •Pregnancy — vasopressin can cause uterine contraction via cross-reactivity at oxytocin receptors; use only when clearly indicated and alternatives (e.g., desmopressin for gestational DI) are not available.
- •Hyponatremia or history of SIADH — vasopressin will worsen free-water retention and hyponatremia, with seizure and cerebral edema risk.
Drug & Supplement Interactions
The clinically significant interactions of native vasopressin converge on three themes: additive vasoconstriction, altered renal water handling, and enhanced endocrine effects. Concomitant catecholamines (norepinephrine, epinephrine) and other pressors (phenylephrine, angiotensin II): by design, vasopressin is often combined with norepinephrine in septic shock, and the combination is synergistic. The clinical task is titrating the combination to achieve target MAP while avoiding cumulative ischemic burden; there is no pharmacologic antagonism to flag, but monitoring intensity must be appropriate. Ganglionic blockers and anesthetics that lower vascular tone: vasopressin's pressor effect can be magnified in a volume-depleted or sympatholytic patient, producing overshoot hypertension. Drugs that promote SIADH or water retention — SSRIs, SNRIs, carbamazepine, oxcarbazepine, vincristine, cyclophosphamide, NSAIDs, chlorpropamide: combined use compounds hyponatremia risk, particularly during prolonged vasopressin infusion or when native vasopressin is used for DI replacement. Loop and thiazide diuretics: complex interaction. Thiazides can potentiate the antidiuretic effect of vasopressin via sodium depletion and increased proximal water reabsorption; loop diuretics can partially blunt renal concentrating ability. Monitoring sodium is essential. Lithium and demeclocycline: these agents induce nephrogenic diabetes insipidus by impairing renal V2 response; vasopressin efficacy for DI may be blunted. Corticosteroids: glucocorticoid deficiency can unmask or worsen vasopressin-induced water retention; in septic shock, concurrent hydrocortisone (as part of the septic shock bundle) is not a contraindication but fluid balance should be tracked. Ganciclovir, foscarnet, and other nephrotoxins: in the ICU population using vasopressin, cumulative renal injury from multiple agents should be monitored, though no direct pharmacokinetic interaction with vasopressin is documented. No significant CYP-mediated interactions are expected, as vasopressin is cleared by peptidases rather than hepatic CYP metabolism.
Safety Profile
Common Side Effects
Cautions
- • ICU-only drug at pressor doses — continuous blood pressure monitoring required
- • Digital and mesenteric ischemia risk increases above 0.03 U/min
- • Not for use as sole pressor — intended as adjunct to norepinephrine in vasodilatory shock
- • Coronary vasoconstriction can precipitate ischemia in susceptible patients
- • Fluid balance and serum sodium must be monitored
What We Don't Know
Well-characterized pharmacology but ongoing uncertainty about optimal timing of initiation, ideal dose ceiling, and which shock subgroups benefit most from vasopressin vs. other second-line pressors.
Legal Status
United States
Vasopressin is FDA-approved as Pitressin (and generic formulations, including Vasostrict) for central diabetes insipidus and for postoperative abdominal distension. It is widely used off-label but consistent with professional guidelines for septic and vasodilatory shock. Prescription-only; not a controlled substance. It is dispensed only to hospitals and healthcare institutions, not retail pharmacies. The V1-selective analogue terlipressin (Terlivaz) received FDA approval in September 2022 for hepatorenal syndrome-1. The V2-selective analogue desmopressin is covered in a separate directory entry.
International
Approved across major markets for similar indications. Terlipressin has a longer European approval history than in the United States and is commonly used for variceal bleeding in addition to hepatorenal syndrome.
Sports & Competition
Native vasopressin is not specifically named on the WADA Prohibited List, but its V2-mediated antidiuretic activity makes it potentially usable for urine dilution/masking in anti-doping testing, which falls under the S5 (Diuretics and Masking Agents) category. Desmopressin is explicitly prohibited. Athletes with legitimate therapeutic need would require a Therapeutic Use Exemption. In practice, ICU-restricted native vasopressin is not a performance-enhancement concern.
Regulatory status changes over time. Verify current local rules with a qualified professional.
Myths & Misconceptions
Myth
Vasopressin and desmopressin are basically the same drug.
Reality
They differ in a clinically dangerous way. Native vasopressin activates V1a receptors (vasoconstriction, pressor effect) at doses comparable to its V2 antidiuretic activity, which is why it is an ICU drug. Desmopressin was engineered specifically to eliminate V1a pressor activity while preserving V2 antidiuresis, which is what makes it safe for ambulatory chronic use in bedwetting and diabetes insipidus. Using native vasopressin outside a monitored setting because 'it's just ADH' is how people get digital ischemia.
Myth
Vasopressin is a first-line vasopressor for septic shock.
Reality
Current Surviving Sepsis Campaign guidance positions norepinephrine as first-line and vasopressin as an add-on when MAP remains inadequate despite rising norepinephrine doses. The VASST and VANISH trials did not show a mortality benefit for vasopressin as a standalone or early strategy. Its role is adjunctive and catecholamine-sparing, not primary.
Myth
Vasopressin should be used instead of epinephrine in cardiac arrest because it lasts longer.
Reality
Multiple meta-analyses and a Cochrane review have found no consistent benefit of vasopressin over or in combination with epinephrine for ROSC, survival to discharge, or neurological outcome in cardiac arrest. Most current advanced cardiac life support algorithms have removed vasopressin as a routine option in favor of epinephrine alone, reflecting the absence of a meaningful mortality or neurological benefit.
Myth
The 'love hormone' story for oxytocin applies equally to vasopressin because they are nearly identical molecules.
Reality
Vasopressin and oxytocin differ by only two amino acids and both have central behavioral effects — the vole pair-bonding literature strongly implicates V1a signaling in male bonding behavior, and human studies show AVP effects on social recognition and aggression. But vasopressin is clinically a water-balance and pressor hormone, not a consumer 'connection' peptide. The receptor distribution, dose-response, and therapeutic index are entirely different from intranasal oxytocin, and treating native vasopressin as a behavioral agent would be both unvalidated and dangerous given V1a pressor effects.
Myth
Copeptin is a new discovery that replaces vasopressin measurement.
Reality
Copeptin is not the hormone itself — it is a stable C-terminal glycopeptide cleaved from the same pre-pro-AVP precursor in equimolar amounts to vasopressin. It has replaced direct AVP measurement in clinical practice because AVP is unstable in plasma and binds to platelets, making immunoassays unreliable. Copeptin is a surrogate, and interpretation still requires appropriate stimulation testing (hypertonic saline or arginine) for AVP-deficiency diagnosis.
Myth
If vasopressin worked for diabetes insipidus, it should work for diabetes mellitus too.
Reality
The shared word 'diabetes' reflects a historical naming artifact (both involve polyuria), not shared physiology. Diabetes insipidus is a disorder of water handling caused by AVP deficiency or AVP resistance; diabetes mellitus is a disorder of glucose handling caused by insulin deficiency or resistance. Vasopressin has no role in diabetes mellitus management. Confusion between the two has caused real clinical errors, which is why the distinction matters in patient education.
Published Research
14 studiesVasopressin in vasoplegic shock in surgical patients: systematic review and meta-analysis
Arginine or Hypertonic Saline-Stimulated Copeptin to Diagnose AVP Deficiency
Terlipressin effect on hepatorenal syndrome: Updated meta-analysis of randomized controlled trials
Terlipressin plus Albumin for the Treatment of Type 1 Hepatorenal Syndrome (CONFIRM)
Wong et al., NEJM 2021 — phase 3 RCT supporting FDA approval of terlipressin (Terlivaz) for HRS-1. 32% verified HRS reversal vs. 17% with placebo, with increased respiratory adverse events.
Vasopressin in septic shock: an individual patient data meta-analysis of randomised controlled trials
A Copeptin-Based Approach in the Diagnosis of Diabetes Insipidus
Fenske et al., NEJM 2018 — hypertonic-saline-stimulated copeptin outperformed the water-deprivation test (95.2% vs. 73.3% accuracy) for distinguishing central DI from primary polydipsia.
Terlipressin versus placebo or no intervention for people with cirrhosis and hepatorenal syndrome (Cochrane)
Effect of Early Vasopressin vs Norepinephrine on Kidney Failure in Patients With Septic Shock: The VANISH Randomized Clinical Trial
Vincent du Vigneaud: following the sulfur trail to the discovery of the hormones of the posterior pituitary gland at Cornell Medical College
Historical account of du Vigneaud's 1950s synthesis of oxytocin and vasopressin at Cornell, which won the 1955 Nobel Prize in Chemistry.
Vasopressin for cardiac arrest: meta-analysis of randomized controlled trials
Neuropeptides and social behaviour: effects of oxytocin and vasopressin in humans
Vasopressin versus Norepinephrine Infusion in Patients with Septic Shock (VASST)
Landmark NEJM 2008 trial (n=778) comparing low-dose vasopressin vs. norepinephrine in septic shock. No overall 28-day mortality difference, but signal for benefit in less-severe stratum.
Physiology of Vasopressin Relevant to Management of Septic Shock
The Pathogenesis of Vasodilatory Shock
Quick Facts
- Class
- Posterior Pituitary Neurohormone
- Evidence
- Strong
- Safety
- Well-Studied
- Updated
- Apr 2026
- Citations
- 14PubMed
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