Section 01
What it's used for
Diabetes Insipidus (Approved)
Desmopressin, brand DDAVP, is the standard approved treatment for central diabetes insipidus, where the body can't make enough ADH, also called vasopressin, the hormone needed to concentrate urine. It replaces that missing hormone.
▸Clinical wording
Desmopressin (DDAVP) is the standard treatment for central diabetes insipidus, replacing deficient ADH.
Septic Shock (Approved)
Used in septic shock, in people, to lower the needed dose of norepinephrine. VASST found it about as effective, not better: 28-day deaths were 35.4% vs 39.3% (P=.26, not significant). Removed from cardiac-arrest guidelines in 2020.
▸Clinical wording
Vasopressin is used in septic shock as a norepinephrine-sparing adjunct; the VASST trial found it noninferior to norepinephrine, with 28-day mortality of 35.4% versus 39.3% (not a statistically significant difference, P=.26), rather than a superior mortality benefit. It is no longer part of the adult cardiac-arrest algorithm in ACLS guidelines, since the 2020 AHA update removed vasopressin after trials showed no advantage over epinephrine alone.
Social Behavior Research
Researchers study whether the receptor vasopressin binds to, called V1a, a docking site for the hormone on cells, affects social behaviors: bonding with a partner, recognizing familiar individuals, and features of autism spectrum disorder.
▸Clinical wording
V1a receptor signaling is studied for pair bonding, social recognition, and autism spectrum disorder.
Hemophilia and von Willebrand
Desmopressin is approved to treat mild hemophilia A and von Willebrand disease, two inherited bleeding disorders. It triggers the body to release its own stored clotting factors, von Willebrand factor and Factor VIII, into the blood.
▸Clinical wording
Desmopressin releases stored von Willebrand factor and Factor VIII for mild hemophilia A and vWD.
Section 02
Mechanism of Action
How the brain senses blood saltiness
- Large hypothalamic neurons make the hormone and release it from their pituitary endings.
- Saltier blood shrinks the cell, and the inward-moving membrane opens a shortened ion channel (TRPV1).
- Cells lacking that channel lose the response, and adding the shortened version restores it.
- Sodium is sensed separately, and all the evidence comes from rat, mouse and guinea pig preparations.
▸Clinical wording
Osmotic control of release from magnocellular neurons
Vasopressin is synthesised in hypothalamic magnocellular neurosecretory cells and released from their neurohypophysial terminals. These cells are intrinsically osmosensitive: hypertonicity shrinks the cell, and inward displacement of the plasma membrane gates an N-terminally truncated TRPV1 variant. Osmosensitivity is absent in Trpv1-null cells and is restored by transfecting the truncated variant, which confers osmotic but not capsaicin responsiveness. Coupling to microtubules is required, and fenestrae in the cortical actin layer amplify the deflection. Sodium is detected separately through the NaX channel encoded by Scn7a. Evidence is from rat, mouse and guinea pig preparations.
Moving water channels to the kidney surface
- In kidney collecting-duct cells this receptor raises the messenger cAMP and activates the kinase PKA.
- PKA tags the water channel AQP2 at one site, the step needed for its surface insertion.
- Mutants that cannot be tagged fail to move, and mice carrying such a change pass excess urine.
- A later tag slows the channel's removal, while the cell's scaffolding clears a delivery path.
▸Clinical wording
V2 receptor cAMP signalling and aquaporin-2 trafficking
In collecting duct principal cells the V2 receptor couples to Gs and adenylyl cyclase, with AC6 the critical isoform since only AC6-null mice show a concentrating defect, raising cAMP and activating PKA held near AQP2-bearing vesicles by A-kinase anchoring proteins. PKA phosphorylates AQP2 at Ser256, the step required for apical insertion: the S256A mutant fails to translocate in LLC-PK1 cells, and mice carrying S256L are polyuric. Later phosphorylation at Ser269 blocks Lys270 ubiquitination and slows endocytosis, while RhoA inactivation and actin depolymerisation clear the path for microtubule- and dynein-driven vesicle delivery.
Squeezing vessels, but not everywhere
- On vessel muscle this receptor releases calcium inside the cell, which drives contraction.
- That calcium-dependent contraction underlies the rise in blood pressure.
- Structural work resolved the human receptor as a pair whose shape changes when a blocker binds.
- In heart and lung vessels the same receptor can instead release nitric oxide and widen them.
▸Clinical wording
V1a receptor Gq signalling in vascular smooth muscle
V1a receptors on vascular smooth muscle couple mainly to Gq/11, driving phospholipase C, inositol trisphosphate, calcium mobilisation and protein kinase C, and this calcium-dependent contraction underlies the pressor response. Cryo-EM of the human receptor resolved it as a homodimer whose ligand-free state carries an unusual flat extracellular loop 2 that remodels on antagonist binding, with dimerisation affecting ligand sensitivity in cells. The vascular response is not uniformly constrictor: in coronary and pulmonary vessels V1a occupancy also elicits nitric oxide, and at low concentrations purinergic receptors mediate endothelial vasodilation.
The stress-hormone partner receptor
- This receptor sits mostly on pituitary cells that release the stress hormone ACTH.
- On its own the peptide is a weak trigger, but it works strongly together with CRH.
- Mice lacking the receptor show blunted stress responses, less aggression and impaired social recognition.
- The receptor's message has also been detected in pancreas and adrenal gland.
▸Clinical wording
V1b receptor on corticotrophs and the stress axis
V1b receptors are most concentrated on anterior pituitary corticotrophs and, like V1a, signal through Gq/11 and phospholipase C. Vasopressin on its own is a weak ACTH secretagogue but acts synergistically with corticotropin-releasing hormone, and the two receptors may physically heterodimerise. Avpr1b-null mice show attenuated ACTH responses to most acute stressors, reduced offensive aggression, and impaired social recognition and temporal-order memory. Receptor transcript has also been detected in pancreas and adrenal gland, with functional correlates reported in pancreatic islets and adrenal medulla.
A brain circuit for social interest
- Light-activating one brain pathway in mice raised the time spent investigating other mice.
- The same stimulation raised anxiety-like behaviour, and a blocking drug cancelled both effects.
- Effects were largely confined to males, whose source region held roughly 40-50% more of these cells.
▸Clinical wording
Central V1a circuits and social behaviour
Vasopressin also acts as a central neuromodulator on its own receptors. Optogenetic stimulation of vasopressin neurons projecting from the bed nucleus of the stria terminalis to the lateral septum in AVP-iCre mice increased time spent investigating conspecifics and increased anxiety-like behaviour on the elevated zero maze; both effects were blocked by infusing a V1a antagonist into the lateral septum. Ex vivo patch-clamp recordings showed biphasic V1a-mediated responses in septal neurons. Effects were largely male-specific, and male BNST contained roughly 40-50% more vasopressin cells.
Section 03
Biological Pathways
- Osmosensing in Magnocellular NeuronsHypertonicity shrinks hypothalamic magnocellular neurons, gating a truncated TRPV1 variant coupled to microtubules to trigger release; sodium is sensed separately via the NaX channel, in rodent and guinea pig work.
- V2/cAMP/PKA/AQP2 Water ReabsorptionIn collecting duct cells, V2 couples to Gs and AC6, raising cAMP and activating PKA anchored near AQP2-bearing vesicles; PKA phosphorylation of AQP2 at Ser256 triggers apical insertion, enabling reabsorption.
- V1a/Gq/PLC VasoconstrictionV1a receptors on vascular smooth muscle couple mainly to Gq/11, driving phospholipase C, calcium mobilization, and PKC-dependent contraction; coronary and pulmonary V1a occupancy can instead elicit nitric oxide.
- V1b/ACTH Stress-Axis SignalingV1b receptors on pituitary corticotrophs signal through Gq/PLC; vasopressin alone is a weak ACTH secretagogue but acts synergistically with CRH, and V1b-null mice show blunted ACTH response and less aggression.
- Central V1a Social & Anxiety CircuitsStimulating vasopressin neurons from the bed nucleus of the stria terminalis to the lateral septum increased social investigation and anxiety-like behavior in mice, an effect blocked by local V1a antagonism.
Section 04
Dosage Information
Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-Gly-NH2 (disulfide: Cys1-Cys6)| Route / system | Context | Range studied | Limitation |
|---|---|---|---|
| Intravenous infusion — shock | FDA label (Vasostrict): septic and post-surgery shock | Septic shock 0.01–0.07 units/min; after heart surgery 0.03–0.1. Steps of 0.005: up every 10–15 min, down hourly. Not dosed by weight. | Titrated against a pressure line in intensive care, added to drugs that already failed. No data above these rates; the label reports gut and limb ischaemia. |
| Intravenous infusion — sepsis trial | 778 patients, compared with norepinephrine | 0.01–0.03 units/min against norepinephrine 5–15 µg/min, both raised to an average blood pressure of 65–75 mmHg. | Deaths at 28 days were 35.4% against 39.3%, a gap within chance. It shows vasopressin is a tolerable substitute at these rates, not that it adds anything. |
| Intravenous push — cardiac arrest | Former resuscitation protocol, dropped in 2015 | 40 units in one push, replacing the first or second dose of adrenaline — against 0.01–0.1 units per minute in shock. | The 2015 guideline update deleted it: added to adrenaline it gave no benefit over adrenaline alone. The number survives only as something tried and dropped. |
| Intranasal / oral — desmopressin | FDA labels, central diabetes insipidus in adults | Spray 10–40 µg a day, one to three doses (10 µg per 0.1 mL). Pills 0.1–1.2 mg a day, two or three; 0.1–0.2 mg lasts up to eight hours. | Desmopressin is another molecule that does not raise pressure, so none of this transfers. Drinking freely causes water poisoning — low sodium, seizures, death. |
| Intranasal — social behaviour tests | Single-dose laboratory studies in healthy adults | 20 IU and 40 IU, single doses. In men, 20 IU lowered how they rated faces, below placebo and 40 IU, and it held on later test days. | The bigger dose did less, and the effect split by V1a receptor gene, so no number here predicts one person. Nothing clinical was measured. |
Results
Syringe Fill Level (100u syringe)
Set positive values for: Recommended dose per kg.
Research Use Only. This information is for educational and research purposes only. Not intended for medical advice or self-medication.
Section 05
Protocols
No protocols featuring this peptide yet. Browse All Protocols
Section 06
Stability & Storage
Storing the product
Vasopressin injection is kept at 2–8 °C or at controlled room temperature. The related analogue desmopressin is supplied as a nasal spray kept at room temperature or as tablets kept at 25 °C. The molecule's disulfide bond is essential for its activity and needs to stay intact.
After opening
A specific in-use period after opening is not given for these products, so they are used within the timeframe stated on their own packaging and kept under the same storage conditions as before opening; anything that could break the disulfide bond, such as harsh oxidation, works against the hormone's stability.
Section 07
Side Effects & Precautions
Vasopressin's reported effects include generally reported reactions, added risks when given intravenously, and a different profile for the related drug desmopressin.
Commonly reported reactions
- Water intoxication or low blood sodium (hyponatremia), from the drug's water-retaining action on the V2 receptor.
- Headache.
- Nausea.
- Abdominal cramps.
Added risks with IV use
- Constriction of the coronary (heart) blood vessels.
- Reduced blood flow to the fingers or toes (digital ischemia) at high doses.
A different profile for desmopressin
Desmopressin, a related drug, has less vasopressor (blood-vessel-constricting) activity because it acts mainly on the V2 receptor.
Section 08
Regulatory Status
Its synthetic analogue desmopressin is a separate approved medicine with a much broader footprint of its own, including a World Anti-Doping Agency restriction that does not apply to vasopressin.
FDA / United States
Approved for vasodilatory shock
Vasostrict (vasopressin injection, USP) was approved on April 17, 2014, to raise blood pressure in adults with vasodilatory shock — for example post-cardiotomy or septic shock — who remain hypotensive despite fluids and catecholamines.
Desmopressin (DDAVP)
Approved separately, in 1978
The FDA cleared desmopressin in February 1978 for central diabetes insipidus, nocturnal enuresis, and bleeding linked to von Willebrand disease or mild haemophilia A; it is a distinct drug from vasopressin, not a brand name for it.
WHO Essential Medicines
Only desmopressin is listed
Desmopressin appears on the WHO Model List of Essential Medicines; vasopressin itself does not, despite being described that way in some older summaries.
WADA
Bans desmopressin, not vasopressin
Desmopressin is named on the 2026 Prohibited List under S5 (diuretics and masking agents), because of its potential to dilute blood parameters used to detect blood doping; vasopressin does not appear anywhere on the list.
«Vasopressin» and «desmopressin» are often used as if interchangeable, but they are two separate approved drugs with two separate labels and two separate anti-doping histories — check which one a product actually contains before relying on either drug's regulatory record.
Section 09
Research Studies
- [1]Mechanisms of intrinsic osmolality and sodium detection by magnocellular neurosecretory neuronsSalgado-Mozo S, Murtaz A, Wyrosdic JC, O'Reilly-Fong J, Zaelzer C, LaPierre MP, Bourque CW · Journal of Neuroendocrinology · 2025
- [2]Molecular mechanisms regulating aquaporin-2 in kidney collecting ductJung HJ, Kwon TH · American Journal of Physiology - Renal Physiology · 2016
- [3]Molecular basis of antagonism of the dimeric human arginine vasopressin receptor 1AZhong P, Chu B, Yu Z, Qiao Y, Ding Y, Zhang Y, Wu X · Nature Communications · 2026
- [4]Bench-to-bedside review: vasopressin in the management of septic shockRussell JA · Critical Care · 2011
- [5]The vasopressin Avpr1b receptor: molecular and pharmacological studiesRoper JA, O'Carroll AM, Young WS 3rd, Lolait SJ · Stress · 2011
- [6]A vasopressin circuit that modulates mouse social investigation and anxiety-like behavior in a sex-specific mannerRigney N, Campos-Lira E, Kirchner MK, Wei W, Belkasim S, Beaumont R, Singh S, Suarez SG, Hartswick D, Stern JE, De Vries GJ, Petrulis A · Proceedings of the National Academy of Sciences of the USA · 2024
Section 10
Frequently Asked Questions
Desmopressin is a synthetic analog that acts almost only on the V2 receptor, giving it strong antidiuretic effects with little of vasopressin's blood-vessel-constricting action — it's used for diabetes insipidus and to release stored clotting factors in mild hemophilia. Vasopressin itself activates V1a, V1b and V2 receptors together, which is why the IV form is used to raise blood pressure in shock rather than just to concentrate urine.
The VASST trial compared them in 778 patients and found vasopressin noninferior, not superior: 28-day mortality was 35.4% versus 39.3% on norepinephrine, a gap that did not reach statistical significance (P=.26). It shows vasopressin is a tolerable norepinephrine-sparing option at the studied infusion rates, not that it improves survival.
It used to be given as a 40-unit push in place of an early epinephrine dose, but the 2015 resuscitation guideline update removed that step, and the 2020 AHA update dropped vasopressin from the adult cardiac-arrest algorithm entirely. Trials found adding it to epinephrine gave no benefit over epinephrine alone.
Because it promotes water retention through V2 receptors, hyponatremia and water intoxication are the main systemic risks, alongside headache, nausea and abdominal cramps. The IV form used in shock can also cause coronary vasoconstriction and, at higher doses, ischemia in the fingers and toes — the FDA label reports gut and limb ischemia even within its listed dose range.
The FDA label for Vasostrict gives 0.01 to 0.07 units per minute in septic shock, titrated against a continuous blood-pressure line in intensive care and typically added only after other pressor drugs have already been tried. It is not dosed by body weight, and no data exist for rates above this labeled range.
It is kept at 2 to 8 °C or at controlled room temperature before use, and its activity depends on an intact disulfide bond that harsh oxidation can break. No specific in-use period after opening is established, so it is used within the timeframe printed on its own packaging.
In single-dose lab studies, intranasal vasopressin at 20 IU made men rate unfamiliar faces less favorably than placebo or a 40 IU dose, an effect that held on later test days. The higher dose did less than the lower one, and the response varied by which version of the V1a receptor gene a person carried — this was a lab measure of face-rating, not a test of real-world bonding.