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Metabolic & endocrine

Vasopressin

The body's own antidiuretic nonapeptide, used intravenously in intensive care to support blood pressure in vasodilatory shock.

L5Practice-changingApproved medicineApprovedHigh confidenceLast reviewed 2026-08-23
IV

Also known as: antidiuretic hormone, ADH, arginine vasopressin, Vasostrict

Evidence passport

Last reviewed 2026-08-23

Evidence level
L5Practice-changing
Confidence
High confidence
Human efficacy
80/100
Human safety
75/100
Regulatory status
Approved medicine
Development
Approved
Routes
IV
Evidence base
Includes human data
Furthest stage
Approved
Source curation
Source curation pending
Clinical maturity
Approved critical-care medicine

Overview

Human evidence80/100
Preclinical evidence75/100
Human safety evidence75/100

Clinical maturity: Approved critical-care medicine

Routes & formulations

Studied / approved routes

IV

The approved context is intravenous infusion in intensive care; there is no approved non-parenteral product for systemic use.

Route availability is not evidence of efficacy, and evidence from one route does not transfer to another. The Registry never provides dosing or sourcing information.

Peptide lifecycle

  1. Discovery

  2. Preclinical

  3. Phase I

  4. Phase II

  5. Phase III

  6. Approved

Approved

What it is

An endogenous nine-amino-acid hormone that constricts blood vessels via V1a receptors and promotes water retention via V2 receptors; synthetic vasopressin is given intravenously in shock states.

What people claim

  • Raises blood pressure in vasodilatory (e.g. septic) shock
  • Reduces catecholamine requirements in critical care

What the evidence actually says

Large randomised trials and decades of critical-care experience established its role as a vasopressor in vasodilatory shock. Its status as a natural hormone sometimes invites extrapolation to wellness contexts for which no evidence exists.

Human evidence

  • Randomised controlled trials in vasodilatory and septic shock.
  • Extensive critical-care haemodynamic and pharmacology data.

Preclinical evidence

  • Vascular and renal receptor pharmacology of V1a/V2 agonism.

Animal and cell findings are Level 1–2 evidence.

Mechanism and pathways

  • V1a-mediated vasoconstriction raises systemic vascular resistance; V2 activity promotes renal water reabsorption.

Safety and unknowns

  • Labelled risks include ischaemic effects from vasoconstriction and hyponatraemia; use is monitored intensive-care therapy.
  • No evidence supports research-market or wellness uses.

Cancer relevance

No concern identified

No established human cancer signal within approved use.

Regulatory status

Approved IV vasopressin products (e.g. Vasostrict) are indicated to increase blood pressure in adults with vasodilatory shock who remain hypotensive despite fluids and catecholamines. Approval is specific to that critical-care context.

Evidence grade

L5Practice-changingHigh confidence

Replicated large randomised trials, pivotal Phase 3 programmes, or a major regulatory decision.

What would change our rating?

  • Not applicable at this evidence tier.

References and sources

Source curation pending
  • To be curatedSources to be curated

Source hierarchy: regulatory documents and trial registries first, peer-reviewed work next, sponsor material flagged as non-independent. We never use supplier or clinic marketing as evidence, and where a verified source has not yet been curated we say so rather than inventing one.

Evidence change history

No recorded changes yet. Baseline position set on 2026-08-23.