ADH is the predominant hormone that regulates the rate of free water excretion. It is a neurohypophyseal polypeptide that is synthesized in the supraoptic and paraventricular nuclei and is secreted after migration to the posterior lobe of the pituitary as a response to the appropriate stimuli. ADH secretion is mainly influenced by the input from the osmotic and volume receptors, with an increase due to hyperosmolality and volume depletion, respectively. But multiple other stimuli play a role such as stress situations, nausea and hypoglycemia. Nicotine and morphine also enhance ADH release.
There are three receptors for ADH, by binding to the V1 receptor vasoconstriction and prostaglandin release occurs; stimulation of the V1b or V3 receptor facilitates the release of adrenocorticotropic hormone (ACTH) in the pituitary. Activation of the V2 receptor mediates the antidiuretic response by fusing the ADH-sensitive water channels, aquaporin-2, with the luminal membrane of the collecting tubules in the nephrons. This process allows water to be reabsorbed down the osmotic gradient towards the systemic circulation across the basolateral membrane. Once the ADH effect has worn off, the water channels return to the cytoplasm after endocytosis.
ADH also appears to affect electrolyte handling by enhancing sodium reabsorption and secretion of potassium in the cortical collecting tubule; however, these effects do not seem to be of major importance in maintaining the electrolyte balance.
(An-Sofie Goessaert, Johan Vande Walle, Ayush Kapila and Karel Everaert- Hormones and Nocturia: Guidelines for Medical Treatment?)
Last date updated on June, 2014