Everyone accepts that the principal physiological action of the neurohypophysial hormone vasopressin is to stimulate the osmotic reabsorption of water by binding to V2 receptors on collecting duct cells. Activation of these G-protein coupled receptors induces the intracellular generation of cyclic AMP and, ultimately, the movement of water across the renal epithelium through water channels inserted into the apical membranes (see Brown 1989). These water channels, called aquaporins, have now been cloned for collecting duct apical membranes in various mammalian species (Fushima et al. 1993).
However, the first observed effect of this antidiuretic hormone was not concerned with the renal action on water transport. In 1895, Oliver and Schäfer showed that extracts of the hypophysis had powerful pressor activity, hence the name given to the active ingredient – vasopressin. Ironically, many people today do not believe that vasopressin has a physiological role in cardiovascular regulation even though it was
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