What is vasopressin? The antidiuretic hormone, explained

What is vasopressin?

Vasopressin, also called antidiuretic hormone or ADH, is a small peptide hormone of 9 amino acids. It is made by nerve cells in the hypothalamus and released from the posterior pituitary, and its main job is telling the kidneys how much water to keep. It also tightens blood vessels.

Vasopressin goes by three names. Its full name is arginine vasopressin, shortened to AVP, and it is also called antidiuretic hormone, or ADH [3], because it reduces how much urine you make. It is a small peptide composed of 9 amino acids [3], the kind of short amino acid chain explained in our peptide basics module.

It is a brain hormone that acts on the body. Specialized neurons in two areas of the hypothalamus, the supraoptic and paraventricular nuclei, make it and send it down to the posterior pituitary gland, which releases it into the blood [1]. Neurons in the same two nuclei also make oxytocin, which differs from vasopressin by only 2 amino acids [1].

How vasopressin tells the kidneys to save water

When blood becomes more concentrated, or blood pressure drops, vasopressin is released. In the kidney it binds V2 receptors and makes cells insert aquaporin-2 water channels, so more water returns to the blood and urine becomes more concentrated. It lasts only about 10 minutes in the blood.

The trigger is mainly concentration. Vasopressin secretion is mainly controlled by extracellular osmolality [3], a measure of how concentrated your body fluids are: it is released when that rises, as it does when you are short of water, and also when pressure sensors detect a fall in blood pressure [3].

In the kidney it works like opening a set of doors. In the collecting ducts, the last stretch of the kidney's tubing, vasopressin acts on V2 receptors [1], and in response, aquaporin-2 water channels stored inside the cells move to the cell surface and raise its water permeability [3]. Water then flows back into the body instead of leaving as urine.

It has other receptors too. Through V1a receptors it contributes to vascular tone, the squeeze of blood vessels, which is where the "vaso" in its name comes from, and through V1b receptors in the pituitary it takes part in the stress response [1]. It is short-lived: vasopressin has a plasma half-life of about 10 minutes [1].

When vasopressin fails: AVP deficiency and AVP resistance

If the brain cannot make enough vasopressin, or the kidneys stop responding to it, people pass large amounts of dilute urine and feel very thirsty. These conditions were called diabetes insipidus; in 2022 an international working group proposed the names AVP deficiency and AVP resistance.

Without enough vasopressin, the kidneys cannot concentrate urine, so people pass large volumes of dilute urine and become very thirsty to keep up [1]. Doctors define that excessive urine as more than 40 mL per kg of body weight a day with urine osmolality below 800 mOsm/kg, and the excessive drinking as more than 3 L a day [1].

There are two main ways it happens. In AVP deficiency, the hypothalamus or posterior pituitary does not release enough hormone; surgery is the most common cause, typically starting 1 to 2 days after pituitary surgery and resolving within 2 to 5 days in most cases [1]. In AVP resistance, vasopressin levels are normal or high but the kidneys are insensitive to it [1].

You may know these conditions by their old name, diabetes insipidus, a term introduced in 1794 to tell these patients apart from those with diabetes mellitus [2]. The shared word "diabetes" has caused confusion that has been to the detriment of patients cared for by non-specialists [2], so in 2022 a working group of endocrine societies proposed renaming them arginine vasopressin deficiency (AVP-D) and arginine vasopressin resistance (AVP-R) [2].

Copeptin: how doctors measure vasopressin

Vasopressin itself is unstable and hard to measure, so doctors measure copeptin, a stable fragment cut from the same precursor. Copeptin measured after a salt-water infusion separates AVP deficiency from excessive drinking with a diagnostic accuracy of 96% to 97%, against 70% to 77% for the older water deprivation test.

Vasopressin is made as a larger precursor, and the piece cut from its end is copeptin, the C-terminal part of pre-pro-vasopressin [1]. Because vasopressin itself is unstable and technically hard to measure, while copeptin is highly stable in blood [1], copeptin has become the practical stand-in.

That changed how the conditions above are diagnosed. The traditional water deprivation test reaches a diagnostic accuracy of only 70% to 77% and is no longer considered the gold standard [1]. Measuring copeptin after a hypertonic (concentrated) salt infusion, with a cutoff of more than 4.9 pmol/L, separates people who simply drink too much from those with AVP deficiency, with a diagnostic accuracy of 96% to 97% in two large prospective studies [1].

Vasopressin and oxytocin: two related peptides

Oxytocin is a close relative of vasopressin. Both are 9-amino-acid peptides made in the same two areas of the hypothalamus and released from the posterior pituitary, and they differ by only 2 amino acids. Oxytocin drives labor and milk release and shapes social behavior; a deficiency of it is only now being recognized.

Vasopressin has a twin. The same two hypothalamic nuclei also make oxytocin, and both hormones leave through the posterior pituitary [1]. Oxytocin is also a nonapeptide, a chain of nine amino acids, and it differs from vasopressin by only 2 of them [1].

Those two amino acids change the job almost completely. Oxytocin plays a central role in labor and lactation, and also influences metabolism, social behavior, emotional processing and stress regulation [1]. Vasopressin, as above, runs water balance and blood vessel tone.

Because they come from the same place, damage to that area can take out both. Oxytocin deficiency has only recently been recognized as a possible condition, mainly in people with hypothalamic or pituitary injury who also have AVP deficiency, and emerging evidence links it to social difficulties, anxiety and lower quality of life [1]. It is hard to diagnose, and treatment with intranasal oxytocin still needs robust randomized trials [1].

Desmopressin: the vasopressin drug

Desmopressin is a modified vasopressin that acts almost only on the kidney's V2 receptors and lasts far longer than vasopressin's roughly 10 minutes. It is the main treatment for AVP deficiency and is also used for bedwetting, where it probably helps more children reach two dry weeks than placebo, though the evidence is low quality.

Desmopressin is a synthetic analogue of vasopressin with two chemical changes, a deaminated cysteine and a D-arginine, which make it highly selective for V2 receptors, with negligible effect on blood vessels, and give it a markedly prolonged half-life [1]. It is the mainstay of treatment for AVP deficiency, and that treatment relies on careful education to avoid both dehydration and hyponatremia [1], a dangerous drop in blood sodium that happens when the body holds on to too much water.

Desmopressin has been used to treat bedwetting since the 1970s [5]. The 2025 Cochrane review pooled 95 studies with 8473 participants [5]. Compared with placebo, desmopressin probably leads to more children achieving 14 consecutive dry nights by the end of treatment [5], but compared with a bedwetting alarm there may be little or no difference [5], and the overall quality of the evidence was low or very low [5].

Vasopressin in septic shock

Hospitals also use vasopressin itself, for its blood vessel effect, alongside other drugs to hold up blood pressure in septic shock. In the VASST trial of 778 patients, adding low-dose vasopressin instead of more norepinephrine did not significantly change 28-day mortality: 35.4% against 39.3%.

The "vaso" side of vasopressin has a medical use too. It is commonly added to the standard blood pressure drugs to support blood pressure in septic shock that does not respond well to them [4]. Whether that saves lives was tested in VASST, a randomized, double-blind trial in which 778 patients already receiving norepinephrine got either low-dose vasopressin or more norepinephrine [4].

There was no significant difference in 28-day mortality, 35.4% with vasopressin and 39.3% with norepinephrine [4], and serious adverse events were similar, 10.3% against 10.5% [4]. In other words, it is used as a blood pressure support, but this trial did not show that it lowers deaths compared with the usual drug [4].