Antidiuretic hormone
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Antidiuretic hormone (ADH) is synthesized in the hypothalmus before being transported via within neurones to the the posterior pituitary gland. ADH is stored in secretory vesicles in the posterior pituitary until it is secreted. It promotes water reabsorption in the late distal convoluted tubule and collecting ducts of the kidneys by the insertion of aquaporin-2 channels.
ADH binding to V1 receptors causes vasoconstriction.
Increases in plasma concentration are detected by osmoreceptors in the hypothalamus which signal the posterior pituitary to release ADH. A fall in plasma volume is detected by barorecptors in the left atrium, aortic arch and carotid which signal the posterior pituitary to release ADH via the vagus nerve. Minor stimulants of ADH release include exercise, angiotensin II and some drugs such as nicotine.
A number of substance inhibit ADH release:
| Notes | Further detail | |
|---|---|---|
| Source | Synthesized in the supraoptic nuclei of the hypothalamus, released by the posterior pituitary | |
| Function | Conserves body water | Promotes water reabsorption in the collecting ducts of the kidneys by the insertion of aquaporin-2 channels |
| Regulation | Increases secretion
Decreases secretion
| Diabetes insipidus (DI) is a condition characterised by either a deficiency of antidiuretic hormone, ADH, (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI) Cranial DI can be treated by desmopressin, an analog of ADH |
ADH summary overview
Anti-diuretic hormone (ADH or vasopressin) is an important hormone in the control of water resorption and volume status. The synthesis of ADH occurs in the supraoptic and paraventricular nuclei in the hypothalamus. It is then transported to the posterior pituitary gland via the neurohypophysial capillaries.Mechanism of action
ADH binds to V2 receptors on renal principal cells in the distal convoluted tubule (DCT) and collecting ducts (CD). It causes a rise in cAMP which stimulates the incorporation of aquaporin-2 channels into the apical membrane. The aquaporin channels allow increased water resorption and retention. As a result urine becomes more concentrated.ADH binding to V1 receptors causes vasoconstriction.
Control of secretion
ADH release is primarily controlled by plasma osmolality and plasma volume.Increases in plasma concentration are detected by osmoreceptors in the hypothalamus which signal the posterior pituitary to release ADH. A fall in plasma volume is detected by barorecptors in the left atrium, aortic arch and carotid which signal the posterior pituitary to release ADH via the vagus nerve. Minor stimulants of ADH release include exercise, angiotensin II and some drugs such as nicotine.
A number of substance inhibit ADH release:
- Alcohol
- Caffeine
- ANP (released when atria are stretched such as in fluid overload)
- Drugs e.g. steroids and ADH receptor antagonists