Antidiuretic Hormone and Vasopressin

Antidiuretic hormone, also called arginine vasopressin, is the principal hormone controlling renal water excretion. Released from the posterior pituitary in response to rising plasma osmolality or falling blood volume, it acts on the kidney to make the collecting duct permeable to water, concentrating the urine and conserving body water. It is the main effector arm of osmoregulation.

Definition

Antidiuretic hormone (arginine vasopressin) is a nonapeptide synthesised in the hypothalamus and released from the posterior pituitary that increases water reabsorption in the renal collecting duct, chiefly by promoting insertion of aquaporin-2 water channels, thereby concentrating urine and defending plasma osmolality.

Scope

This topic covers the synthesis, release, and renal action of vasopressin, including its control of aquaporin water channels, and the stimuli that govern its secretion. It is a physiological reference for how the hormone regulates water balance; it does not address pharmacological use or the management of vasopressin-related disorders.

Core questions

• Where is vasopressin made and how is it released?
• What stimuli increase or suppress vasopressin secretion?
• How does vasopressin change water permeability in the collecting duct?
• How does the hormone fit into the osmoregulatory feedback loop?

Key concepts

• Arginine vasopressin (ADH)
• Posterior pituitary release
• Osmotic and volume stimuli for secretion
• V2 receptor signalling
• Aquaporin-2 trafficking
• Urine concentration and free water reabsorption
• Set point for vasopressin release

Mechanisms

Vasopressin is synthesised in magnocellular neurons of the hypothalamus and transported to the posterior pituitary, from which it is released into the circulation. A small rise in plasma osmolality sensed by osmoreceptors, or a substantial fall in blood volume or pressure sensed by baroreceptors, increases its secretion. In the kidney, vasopressin binds V2 receptors on collecting-duct principal cells and, through a cyclic-AMP signalling cascade, drives the insertion of aquaporin-2 water channels into the apical membrane; water then follows the medullary osmotic gradient out of the tubule, concentrating the urine. When osmolality falls, vasopressin secretion is suppressed, aquaporin-2 channels are removed, and dilute urine is excreted (knepper-2015, agre-2002, danziger-2015, boron-2017).

Clinical relevance

Deficient vasopressin action produces inability to concentrate urine and water loss, whereas inappropriate excess leads to water retention and dilutional hyponatremia; the syndrome of inappropriate antidiuresis is a recognised example. This entry describes the normal physiology that such disorders disturb and is not a diagnostic or treatment resource; clinical guidance on related sodium disorders is addressed in dedicated guidelines (spasovski-2014).

Evidence & guidelines

The hormone's physiology and its molecular mechanism through aquaporin-2 are established in mechanistic reviews and physiology texts (knepper-2015, agre-2002, boron-2017). Clinical practice guidelines on hyponatraemia incorporate vasopressin physiology when classifying and approaching water-retention states (spasovski-2014).

History

An antidiuretic principle of the posterior pituitary was recognised early in the twentieth century, and the vasopressin peptide was later sequenced and synthesised. The molecular basis of its renal action was clarified by the discovery of aquaporin water channels, which earned Peter Agre a share of the 2003 Nobel Prize in Chemistry and explained how vasopressin controls collecting-duct water permeability (agre-2002, knepper-2015).

Key figures

• Mark Knepper
• Søren Nielsen
• Peter Agre
• Daniel Bichet

Seminal works

• knepper-2015
• agre-2002

Frequently asked questions

What triggers the release of antidiuretic hormone?

A rise in plasma osmolality detected by hypothalamic osmoreceptors is the main trigger; a large fall in blood volume or pressure sensed by baroreceptors also stimulates release, even overriding osmotic signals when volume is severely depleted.

How does vasopressin concentrate the urine?

It acts on V2 receptors in the collecting duct to insert aquaporin-2 water channels into the cells lining the tubule, allowing water to be reabsorbed down the medullary osmotic gradient so that a smaller volume of more concentrated urine is excreted.