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Vasopressin (Vasostrict)9 residuesCYFQNCPRGEach bubble = one amino acid. Size = residue mass. Color = chemical class.Also known as: AVP, ADH, Antidiuretic Hormone
Vincent du Vigneaud won the 1955 Nobel Prize for synthesizing this nine-amino-acid hormone. Vasopressin (arginine vasopressin, AVP, antidiuretic hormone/ADH) is your body's primary blood pressure regulator during shock states. The VASST trial (778 patients)[1] and VANISH trial (409 patients)[2] established its role as an adjunctive vasopressor in septic shock. Vasostrict received FDA approval in 2014 for vasodilatory shock in adults. This is strictly a hospital ICU drug, administered by continuous intravenous infusion under direct physician supervision. No self-administration community exists, and none should.
Two randomized controlled trials on 1,187 critically ill patients form the evidence base. That is a strong clinical foundation for a vasopressor, and vasopressin's data stands alongside the best-studied ICU drugs in use today. Vasopressin (arginine vasopressin, AVP, antidiuretic hormone, ADH; CAS 113-79-1) is a cyclic nonapeptide with the sequence Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-Gly-NH2 and a disulfide bridge between positions 1 and 6. The hypothalamus synthesizes it as a preprohormone, and the posterior pituitary releases it when plasma osmolality rises or blood pressure drops. The mechanism splits across three receptor pathways. V1a receptors on vascular smooth muscle drive vasoconstriction. V2 receptors on renal collecting duct cells promote water reabsorption through aquaporin-2 channels. V1b receptors in the anterior pituitary stimulate ACTH release. That triple action makes vasopressin effective even when catecholamine receptors are downregulated in prolonged shock. The VASST trial (Russell et al., NEJM 2008, n=778) found no overall mortality difference versus norepinephrine, but showed a survival benefit in less severe septic shock (APACHE II 20 to 29). VANISH (Gordon et al., JAMA 2016, n=409) showed a vasopressin-first strategy reduced the need for renal replacement therapy. Surviving Sepsis Campaign 2021 guidelines recommend adding vasopressin at 0.03 U/min when norepinephrine exceeds 0.25 mcg/kg/min. Vasostrict (Par Pharmaceutical) holds the FDA approval, with generic competition from Eagle Pharmaceuticals and American Regent entering in 2022 to 2023.
V1a receptors sit on vascular smooth muscle, hepatocytes, and platelets. When vasopressin binds V1a, the Gq protein activates phospholipase C. This generates inositol trisphosphate (IP3) and diacylglycerol (DAG). IP3 triggers calcium release from the sarcoplasmic reticulum, causing smooth muscle contraction and vasoconstriction. That calcium-driven squeeze on blood vessels is the primary vasopressor effect in shock states. Vasopressin also blocks nitric oxide-mediated vasodilation. In septic shock, pathological overproduction of NO drives refractory hypotension. Catecholamine receptors become downregulated after prolonged exposure to endogenous adrenaline and noradrenaline. Vasopressin bypasses that problem entirely; V1a receptors operate through a separate signaling cascade that remains responsive when adrenergic pathways fail. V2 receptors on the basolateral membrane of renal collecting duct principal cells couple to Gs proteins. The downstream signal activates adenylyl cyclase, raising intracellular cAMP. Protein kinase A then phosphorylates aquaporin-2 water channels and moves them to the apical membrane. Water permeability increases dramatically. This is the antidiuretic mechanism that gave vasopressin its alternate name, ADH. V2 activation on vascular endothelium also releases von Willebrand factor multimers and coagulation Factor VIII from Weibel-Palade bodies. V1b receptors in the anterior pituitary stimulate ACTH secretion through the Gq/PLC pathway. Vasopressin works with corticotropin-releasing hormone (CRH) to amplify the hypothalamic-pituitary-adrenal axis response during physiological stress.
FDA-approved (Vasostrict, 2014) vasopressor for vasodilatory shock. VASST (NEJM 2008, n=778) showed no overall mortality difference vs. norepinephrine but a survival benefit in less severe septic shock (APACHE II 20–29). VANISH (JAMA 2016, n=409) showed vasopressin-first strategy reduced kidney failure (fewer patients requiring CRRT) vs. norepinephrine-first, with no mortality benefit. SSC 2021 guidelines recommend vasopressin as a second-line vasopressor at 0.03 U/min when MAP target not met on norepinephrine alone.
VASST (Russell et al., NEJM 2008, PMID 18305265, n=778); VANISH (Gordon et al., JAMA 2016, PMID 27483065, n=409)
No overall mortality benefit in VASST or VANISH. Benefit restricted to less severe septic shock subgroup in VASST. VANISH primary endpoint (renal failure) showed trend but was underpowered for mortality. Optimal timing, dose, and patient selection remain debated. All evidence is from ICU RCTs: no outpatient or community data exists by definition.
No consumer or self-administration community exists. Vasopressin is an ICU-only continuous IV infusion drug. "Community" context consists entirely of clinical professionals (ICU nurses, critical care physicians) in r/nursing, r/medicine, and r/criticalcare: discussing clinical protocols, not self-use. There is no self-administration market or compounding interest.
No consumer community exists. Vasopressin is exclusively administered by ICU clinicians. Within the scientific community, VASST and VANISH are aligned on adjunctive use alongside catecholamines at 0.01–0.07 U/min; SSC 2021 guidelines codify this as a weak recommendation with moderate-quality evidence. No divergence between trials and current practice guidelines on core dosing.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 0.01 IU | Daily |
| Moderate | 0.03 IU | Daily |
| Aggressive | 0.04 IU | Daily |
Vasopressin is not a self-administration peptide. Everything here applies to ICU clinicians managing the drug on a ventilated or monitored patient. Standard ICU concentration is 0.1 U/mL. Dilute 25 units into 250 mL of 0.9% normal saline or D5W. At that concentration, 0.01 U/min equals 6 mL/hr, 0.03 U/min equals 18 mL/hr, and 0.04 U/min equals 24 mL/hr on the infusion pump. Premixed bags are available at 0.2, 0.4, and 0.6 U/mL concentrations. Use them when possible. The 20 U/mL concentrate vials look similar to the diluted infusion bags, and medication errors from that confusion are documented. Smart pump drug libraries reduce rate-programming errors. Never bolus vasopressin; it causes severe acute hypertension and myocardial ischemia. Start the taper once MAP holds at 65 mmHg for 8 hours without catecholamines. Reduce by 0.005 U/min every 15 to 30 minutes and monitor sodium and urine output for 24 to 48 hours after the infusion stops completely.
Vasopressin is used acutely in critical care settings, not cycled. Continuous IV infusion is titrated to hemodynamic targets and tapered gradually when the patient stabilizes. Typical duration of use ranges from hours to several days. Abrupt discontinuation should be avoided due to the risk of rebound hypotension and transient diabetes insipidus.
Vasopressin is not cycled. It is used acutely in critical care settings as a continuous IV infusion for hours to several days until hemodynamic stability is achieved. The drug is then tapered gradually rather than cycled. Prolonged infusion (>72–96h) does cause V2 receptor downregulation in the kidney (accounting for transient DI on discontinuation) but this is managed by tapering, not cycling off-and-on. No hormonal axis recovery or receptor desensitization concern applies in the context of short-duration ICU use.
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Expected: Restoration of MAP ≥65 mmHg; reduction in norepinephrine requirements; potential reduction in renal replacement therapy need (VANISH signal)
Monitor: Continuous arterial line blood pressure monitoring mandatory. Hourly urine output. Daily serum sodium and electrolytes. Monitor for digital ischemia (finger/toe color and temperature). Abdominal assessment for mesenteric ischemia signs.
Peripheral IV is acceptable only for short durations (under 30 to 60 minutes) when central access is not available.
Dilute 25 units of vasopressin concentrate (20 U/mL) into 250 mL of 0.9% normal saline or D5W for a final concentration of 0.1 U/mL. Alternatively, use a premixed bag (0.2, 0.4, or 0.6 U/mL).
Set the infusion pump to 6 mL/hr (0.01 U/min at 0.1 U/mL concentration). Do not administer as a bolus under any circumstances.
Titrate upward by 0.005 U/min (3 mL/hr increments at 0.1 U/mL) every 10 to 15 minutes until MAP reaches 65 mmHg or higher.
For postcardiotomy shock: 0.1 U/min (60 mL/hr). Rates above 0.04 U/min carry raised ischemic risk.
Monitor continuously: arterial blood pressure, hourly urine output, serum sodium every 12 to 24 hours, digital perfusion every 2 to 4 hours, and daily abdominal assessment.
Decrease by 0.005 U/min every 15 to 30 minutes. Never stop abruptly.
Post-discontinuation: monitor sodium and urine output for 24 to 48 hours. Watch for transient diabetes insipidus (sudden polyuria and hypernatremia) in approximately 1.5% of patients.
Standard dosing 0.01–0.07 U/min (septic shock) or 0.03–0.1 U/min (postcardiotomy)
Dedicated central line strongly preferred. Extravasation from peripheral IV causes local tissue necrosis. Premixed 0.2/0.4/0.6 U/mL bags designed for central administration.
Same dosing; higher extravasation risk
Peripheral IV acceptable in emergencies when central access not immediately available. Limit to ≤30–60 min. Monitor site continuously. Switch to central line as soon as possible. Extravasation antidote: phentolamine 5–10 mg SC in 10 mL NS at site.
Unpredictable absorption; not studied for vasodilatory shock
FDA label lists IM/SC for non-shock indications (e.g., diabetes insipidus) but not used in critical care shock management. Onset delayed and bioavailability variable: unsuitable for hemodynamic emergencies.
Standard combination in septic shock. Vasopressin acts via V1a receptor (non-adrenergic) allowing norepinephrine dose reduction (catecholamine-sparing). VASST and VANISH both used this combination. SSC 2021 recommends adding vasopressin at 0.03 U/min when NE >0.25 mcg/kg/min.
Vasopressin 0.03 U/min + norepinephrine; titrate norepinephrine down as MAP allows
VANISH trial included a 2×2 factorial arm for hydrocortisone. SSC 2021 recommends IV hydrocortisone 200 mg/day in patients with septic shock not responding to fluids and vasopressors. Often co-administered with vasopressin as standard septic shock management.
IV hydrocortisone 200 mg/day (50 mg q6h or continuous infusion) alongside vasopressin
Amplify antidiuretic (V2) effect of vasopressin, dramatically increasing risk of severe hyponatremia and fluid overload. May also potentiate pressor effect unpredictably.
Do not combineAntagonize vasopressin V2 receptor activity, reducing antidiuretic effect and potentially blunting vasopressor response. May require higher vasopressin doses to achieve hemodynamic targets.
NSAIDs prolong and potentiate both vasopressin pressor and antidiuretic effects, increasing ischemia risk and risk of hyponatremia.
Pricing updated 2026-04-09
Peripheral ischemia is the most serious concern. Vasopressin's V1a-mediated vasoconstriction can cause digital ischemia, presenting as finger or toe blanching, cyanosis, and in severe cases, skin necrosis or gangrene. Infusion rates above 0.04 U/min carry significantly raised risk. Mesenteric ischemia is the other major danger, presenting as abdominal pain, ileus, or bowel necrosis. Both complications require immediate dose reduction or discontinuation. Cardiac effects include decreased cardiac output, bradycardia, and tachyarrhythmias. Patients with coronary artery disease face particular risk of myocardial ischemia. The FDA label carries explicit warnings about ischemic complications across all vascular territories. Hyponatremia results from excessive water retention mediated by V2 receptor activation. Serum sodium should be checked every 12 to 24 hours during infusion. If sodium drops below 130 mEq/L, free water restriction and dose reduction are standard interventions. Transient diabetes insipidus develops in approximately 1.5% of patients after abrupt discontinuation. Prolonged infusion causes V2 receptor downregulation in the kidneys. Stopping the drug suddenly leaves those downregulated receptors unable to respond to endogenous ADH, producing sudden polyuria and rising sodium levels. This is precisely why vasopressin must be tapered, never stopped cold. Rebound hypotension accompanies the V2 problem because vascular tone takes time to compensate without exogenous support. Other reported effects include nausea, vomiting, abdominal cramping, headache, vertigo, and bronchospasm. Extravasation at the IV site causes local tissue necrosis due to the extreme vasoconstrictive potency; treat with subcutaneous phentolamine 5 to 10 mg in 10 mL normal saline at the site. Contraindications: known hypersensitivity to 8-L-arginine vasopressin, coronary artery disease at risk for myocardial ischemia, peripheral vascular disease at risk for limb ischemia, and chronic nephritis with raised blood nitrogen. Pregnancy is FDA Category C; vasopressin may produce tonic uterine contractions threatening pregnancy continuation. It is excreted in breast milk. When to stop: progressive digital ischemia despite dose reduction, any suspicion of mesenteric ischemia, myocardial ischemia (troponin rise, ECG changes), or refractory hyponatremia below 125 mEq/L.
Verify Vasopressin (Vasostrict) dosing and safety with a second opinion
FDA-approved pharmaceutical product (Vasostrict) with generic equivalents available. Produced under FDA cGMP regulations, hospital-dispensed only. No compounding risk in current market (compounding effectively eliminated post-2014 NDA). Premixed ready-to-use formulations (0.2/0.4/0.6 U/mL) reduce dilution errors.
| Test | When | Target |
|---|---|---|
| Arterial blood pressure (MAP) | Continuous during infusion | MAP ≥65 mmHg (or per institutional protocol) |
| Urine output | Hourly during infusion | ≥0.5 mL/kg/hr |
| Serum sodium (Na+) | q12–24h during infusion; daily for 24–48h post-taper | 135–145 mEq/L |
| Serum electrolytes panel | Daily during infusion | — |
| Digital/extremity perfusion assessment | q2–4h during infusion, especially at doses >0.04 U/min | — |
| Abdominal assessment (clinical) | Daily and PRN during infusion | — |
Primary therapeutic target; vasopressin titrated to MAP ≥65 mmHg
Antidiuretic V2 effect reduces urine output; oliguria may reflect ischemia vs. therapeutic effect
Hyponatremia risk from V2-mediated water retention during infusion; hypernatremia risk (transient DI) post-discontinuation
Comprehensive electrolyte management in critically ill patients on vasopressors
V1a-mediated vasoconstriction can cause digital ischemia, skin necrosis, and limb-threatening ischemia at higher doses
Mesenteric ischemia risk: abdominal pain, distension, or ileus may indicate bowel ischemia requiring dose reduction or discontinuation
Rapid onset of vasopressor effect with measurable increase in mean arterial pressure
Hemodynamic stabilization with dose titration; reduction in catecholamine requirements
Sustained vasopressor effect at steady-state infusion; antidiuretic effect with reduced urine output
Continued hemodynamic support; monitor for ischemic complications and hyponatremia
Effects resolve within minutes of stopping infusion; monitor for rebound hypotension and transient diabetes insipidus
Minutes 0 to 5: V1a receptor vasoconstriction begins almost immediately. Blood pressure rises on the arterial line monitor within 1 to 5 minutes of starting the infusion at 0.01 U/min. Some patients develop bradycardia; skin blanching at the infusion site is common. Minutes 5 to 30: The ICU team titrates the rate upward toward MAP 65 mmHg. Norepinephrine dose reduction typically starts during this window. The antidiuretic V2 effect kicks in, and urine output drops. Nausea and abdominal cramping can appear. Hours 1 to 6: Steady-state vasopressor effect establishes at the target infusion rate. Catecholamine requirements decrease measurably. Antidiuretic activity stabilizes. Nursing staff should begin watching for early signs of digital or peripheral ischemia and checking serum sodium. Hours 6 to 96: The median vasopressin infusion in VASST lasted 3 days. During this window, monitoring shifts toward ischemic complications (digital ischemia, mesenteric ischemia presenting as abdominal symptoms) and electrolyte disturbances (hyponatremia from V2-mediated water retention). Post-discontinuation (taper phase): The 10 to 20 minute half-life means pharmacological effects clear within minutes of stopping the pump. The risks shift to rebound hypotension during the taper and transient diabetes insipidus from V2 receptor downregulation in roughly 1.5% of patients. Polyuria and rising sodium levels can persist for 1 to 5 days. Monitor urine output and sodium for at least 24 to 48 hours after the infusion stops.
Rapid V1a receptor-mediated vasoconstriction; measurable MAP increase within 1–5 minutes of starting infusion at 0.01 U/min
N/A: ICU-administered; nursing staff observe hemodynamic response on monitors
Dose titration to MAP target (≥65 mmHg); norepinephrine dose reduction begins; antidiuretic effect reduces urine output
N/A
Sustained vasopressor effect at steady-state infusion rate; catecholamine requirements decrease; antidiuretic V2 effect stabilizes
N/A
Continued hemodynamic support; VASST median vasopressin infusion was 3 days; monitor for ischemic complications and electrolyte disturbances
N/A
Effects resolve within minutes of stopping infusion (t½ 10–20 min); risk of rebound hypotension during taper; V2 receptor downregulation may cause transient DI in ~1.5% of patients lasting 1–5 days
N/A
Source: FDA label and Czaczkes et al. (1964) PMID 1262458: plasma half-life 10-20 minutes IV
Loading the interactive decay curve.
Vasopressin injection received FDA approval in 2014 under NDA 204485 as Vasostrict, manufactured by Par Pharmaceutical (Endo International). It is approved for the treatment of vasodilatory shock in adults who remain hypotensive despite fluid resuscitation and catecholamines. Generic equivalents from Eagle Pharmaceuticals and American Regent became available in 2022 to 2023, reducing hospital acquisition costs by approximately 50% from peak brand pricing. Before 2014, vasopressin was distributed as an unapproved compounded drug at roughly $1 per dose. The post-approval price reached approximately $158 per dose by 2022, drawing congressional scrutiny. Vasopressin is a Schedule VI (non-controlled) prescription medication. It is available only through hospital pharmacies for inpatient use. There is no consumer market, no compounding pharmacy availability for outpatient use, and no self-administration indication. WADA status is not applicable for this drug. This content is for educational reference only. Vasopressin therapy requires direct physician supervision with continuous hemodynamic monitoring in an ICU setting.
Peptide Schedule Research TeamReviewed Apr 20266 Citations
