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Vasopressin
Vasopressin (Vasostrict) is the real, native antidiuretic hormone itself, approved as a drug for vasodilatory shock — distinct from the site's desmopressin (V2-selective) and terlipressin (a longer-acting V1-leaning analog) pages, since native vasopressin hits both receptor types at once, and its own major trial produced a genuinely neutral result.
On this page
In brief
Should you care? Only relevant in an ICU/vasodilatory-shock context — not a wellness product.The short version
- The native, unmodified hormone itself — not an analog, unlike desmopressin or terlipressin elsewhere on this site.
- VASST, its major trial, found no significant mortality benefit over norepinephrine (35.4% vs. 39.3%, p=0.26) — a genuinely neutral result, not a clear win.
- Approved (modern NDA) in 2014 for vasodilatory shock — though synthetic vasopressin has been marketed in some form since the 1920s-40s.
The same hormone, used non-selectively
Vasopressin is the real, native 9-amino-acid antidiuretic hormone (ADH) your body already makes — not an engineered analog. It acts at three receptor types at once: V1a (vascular smooth muscle, causing vasoconstriction), V2 (kidney collecting duct, causing water retention), and V1b (pituitary, ACTH release). That non-selectivity is exactly what distinguishes it from the two analogs already on this site: desmopressin is engineered for near-pure V2 selectivity (antidiuretic effect, minimal pressor effect), while terlipressin is a longer-acting prodrug that leans V1-selective for sustained vasoconstriction. Native vasopressin does both jobs simultaneously, which is exactly why it's used as a blood-pressure-supporting drug in shock despite being "just" the hormone the body already produces.
The VASST trial: a real, neutral result
The modern, formally FDA-approved version (Vasostrict) received its NDA approval on 17 April 2014, for adults with vasodilatory shock who remain hypotensive despite fluids and catecholamine vasopressors — though older, pre-modern-approval-standard vasopressin products go back decades further. Its central trial, VASST (Russell et al., N Engl J Med 2008, PMID 18305265), is worth reading precisely because the result is genuinely neutral: 778 patients with septic shock, randomized to low-dose vasopressin or norepinephrine added to open-label catecholamines. 28-day mortality was 35.4% with vasopressin versus 39.3% with norepinephrine (RR 0.90, 95% CI 0.75-1.08, p=0.26) — not statistically significant. A pre-specified subgroup of patients with less severe shock showed a possible benefit (90-day mortality 35.8% vs. 46.1%, p=0.04), but that's a subgroup finding, not the trial's confirmed primary result, and shouldn't be read as more definitive than it is.
Safety
Because vasopressin constricts blood vessels broadly, not just where needed, it carries a real risk of reduced blood flow to the gut (mesenteric ischemia) and fingers/toes (digital ischemia) — documented in case-series and pharmacovigilance literature, though absolute rates are low and weren't statistically significant in VASST itself (digital ischemia 2.0% vs. 0.5%, p=0.11).
Current status
Still marketed (branded Vasostrict and generic vasopressin injection); has experienced documented US drug shortages at various points. Hospital/ICU-only use, no wellness or grey-market presence.
References
- Russell JA, Walley KR, Singer J, et al. (VASST Investigators), "Vasopressin versus Norepinephrine Infusion in Patients with Septic Shock," N Engl J Med 2008;358(9):877-887, PMID 18305265, DOI: 10.1056/NEJMoa067373.
- FDA approval history for Vasostrict (vasopressin), NDA 204485, 17 April 2014.