Vasopressin

Vasopressin is a small peptide hormone made up of nine amino acids that acts both as a circulating hormone and, within the brain, as a signaling molecule ^[2]. It is produced by nerve cells in the hypothalamus, in particular the supraoptic and paraventricular nuclei, and is carried along their axons to the posterior pituitary gland, where it is stored and released into the bloodstream ^[2]. The hormone is also known as antidiuretic hormone, a name that reflects its central role in controlling how much water the body retains ^[1][2].

Vasopressin acts through several receptor subtypes distributed across different tissues ^[1]. Acting on V2 receptors in the kidney, it drives the reabsorption of water and concentrates the urine, which is its dominant effect at normal physiological levels ^[2]. Acting on V1-type receptors in blood vessels, it causes vasoconstriction and raises blood pressure, an effect that becomes prominent at higher concentrations, while receptors in the pituitary help regulate release of the stress hormone ACTH ^[1][2]. Through these actions the hormone takes part in controlling the body's water balance, blood volume and circulation ^[2].

Vasopressin was among the first peptide hormones to be chemically synthesized, a landmark achieved in the 1950s by Vincent du Vigneaud, and for many years its medical use was largely confined to diabetes insipidus and bed-wetting ^[2]. More recently it has become an important drug in critical care ^[2]. Low doses are given to support blood pressure in catecholamine-resistant vasodilatory and septic shock, where studies found that patients in shock can develop a relative vasopressin deficiency and often respond to its infusion with a reduced need for other vasopressors ^[1]. It is also used during cardiopulmonary resuscitation and to manage certain kinds of bleeding ^[2].

Clinical trials have examined whether vasopressin improves survival in septic shock; a large randomized comparison with norepinephrine found no overall difference in mortality, although it supported the drug's value as a catecholamine-sparing agent ^[3]. Several longer-acting synthetic analogues have been developed for particular uses, including desmopressin for diabetes insipidus and bed-wetting and terlipressin as a vasoconstrictor ^[2]. Vasopressin is a prescription medicine given by injection or infusion, generally in hospital settings, and its effects are short-lived because it is broken down quickly in the body ^[1][2].

Because it constricts blood vessels and retains water, vasopressin can raise blood pressure and cause dangerous low sodium (hyponatremia) from water retention. Intranasal use for cognition, which circulated years ago, carries these same risks. This is a prescription hormone and not appropriate for casual nootropic use. Anyone with cardiovascular disease, kidney issues, or electrolyte problems should never touch it outside medical care.

Vasopressin is given in settings where several vasoactive drugs are running at once, and its pressor effect is additive with catecholamines such as norepinephrine and epinephrine.

Indomethacin more than doubles the time it takes for vasopressin's hemodynamic effect to wear off in healthy volunteers, prolonging its action on cardiac index and systemic vascular resistance; loss of prostaglandin-mediated vasodilation is the likely reason. Ganglionic blocking agents increase the pressor response by roughly a fifth. Furosemide amplifies the renal side of the drug instead, raising osmolar clearance several-fold and urine flow further still.

Drugs that themselves provoke inappropriate ADH secretion, including SSRIs, tricyclics, haloperidol and carbamazepine, tend to increase the pressor effect. Drugs associated with drug-induced diabetes insipidus, notably lithium and heparin, tend to reduce it. Neither direction is large enough to be predictable in an unstable patient, which is why hemodynamic monitoring carries the decision.

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