Vasopressin (ADH; antidiuretic hormone) is normally released by the posterior pituitary gland in response to a fall in blood volume or a rise in plasma osmolality, and plays a major role in the regulation of water reabsorption in the kidney. ADH increases the permeability to water of the distal convoluted tubules and collecting ducts through insertion of aquaporin water channels into the apical membrane of renal tubular epithelial cells [62]. Alcohol also acts directly to inhibit the release of vasopressin. Murray [63] showed that administration of a posterior pituitary extract inhibited alcohol-induced diuresis, and it is widely accepted that alcohol exerts its diuretic action by inhibiting vasopressin release. Elegant work by the groups of Lemos and Treistman [64] showed that this effect occurs in vitro in preparations of isolated nerve terminals at alcohol levels as low as 10mM and Dopico and others have provided a cellular and molecular level explanation for this action of alcohol, in terms of its ability to enhance the opening of Ca2+-activated K+ (BK) channels and thereby reduce the release of vasopressin [65] reviewed in [66].
