At a glance
| Peptide length | 9 amino acids |
|---|---|
| US shock product | Vasostrict |
| Vascular receptor | V1 |
| Water-balance receptor | V2 |
| Approved setting | Vasodilatory shock despite fluids and catecholamines |
Overview
Vasopressin is also known as antidiuretic hormone and is released naturally from the posterior pituitary. Its two prominent actions—constricting blood vessels and conserving water—explain different physiologic and clinical contexts. The current Vasostrict indication is a monitored shock intervention, not a general treatment for dehydration or low energy. In distributive shock, insufficient vascular tone may persist despite conventional resuscitation and catecholamine therapy. Adding vasopressin provides another receptor pathway. Trials have examined whether this translates into better survival, but a blood-pressure response and a mortality benefit are distinct outcomes. Desmopressin is a separately modified analog with different receptor emphasis and product indications.
How it works
Vasopressin activates V1 receptors on vascular smooth muscle through phospholipase-C and calcium-dependent signaling, producing vasoconstriction. V2 receptor activation in the kidney promotes water reabsorption. The vascular action supports blood pressure in shock, while excessive vasoconstriction can compromise blood flow to organs and extremities. Changes in water retention and rebound loss of antidiuretic activity help explain sodium disturbances during or after treatment.
An additional pressor pathway
Vasostrict is labeled for adults with vasodilatory shock who remain hypotensive despite fluid and catecholamine treatment. It is given in a setting with intensive hemodynamic observation. The underlying infection, inflammatory state, or postoperative cause still requires treatment; the peptide supports circulation rather than resolving every cause of shock.
Supporting sources [1]
What VASST showed
The VASST trial compared low-dose vasopressin with norepinephrine added to existing vasopressors in septic shock. It did not demonstrate a significant overall 28-day mortality difference. Subgroup observations generated further hypotheses, but the overall result should not be rewritten as a universal survival advantage from vasopressin.
Supporting sources [2]
Pressure and perfusion can move differently
Recognized problems include reduced cardiac output, arrhythmia, coronary or other ischemia, and water-balance effects. The label also describes reversible diabetes insipidus after discontinuation, with increased urine output and hypernatremia. Monitoring must therefore extend beyond the momentary arterial-pressure reading and include the treatment transition.
Supporting sources [1]
Is vasopressin equivalent to desmopressin?
No. Desmopressin is structurally modified to emphasize antidiuretic activity and reduce vasopressor effects; its approved roles include specific water-balance and bleeding disorders. Native-sequence vasopressin used in shock has a different therapeutic objective and risk balance. The products and administration contexts are not interchangeable.
Supporting sources [1]
Reading this profile
Jurisdiction: United States; indications and availability vary by formulation and country.. Molecular class: Endogenous cyclic nonapeptide hormone; synthetic vasopressor medicine.
This profile was written with AI-assisted research and checked against the linked sources. It has not been represented as a clinician’s review. Evidence summaries describe the cited studies and products; they do not establish that a separately purchased preparation is equivalent.
Sources & references
Follow the original material. Product labels define specific formulations and uses; trial registration describes a study and does not by itself establish benefit.
- Vasostrict — US prescribing information ↗Regulatory source · Checked 2026-10-27
- Vasopressin versus norepinephrine infusion in patients with septic shock. ↗Original research · Checked 2026-10-27