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Correspondence: Sei Sasaki MD, Second Internal Medicine, School of Medicine, Tokyo Medical and Dental University, 1 5 45, Yushima, Bunkyo Ku, Tokyo 113, Japan. Top of pageAbstractThe ability to concentrate the urine was an essential step in the adaptation of animals to life in a terrestrial environment. Only mammals and birds produce a urine which is hypertonic to plasma. A concentrated urine is formed in the kidney collecting duct in response to vasopressin by the massive reabsorption of water from luminal fluid. The most prominent feature of water transport in the collecting duct is the rapid and large change in water permeability induced by vasopressin. In isolated perfused rabbit collecting duct segments, for example, the lag time between the addition of vasopressin and the appearance of an increase of water permeability is less than 30 seconds [1], and more than 10 fold increases in water permeability have been reported [2, 3]. The mechanisms responsible for this drastic change in water permeability have been studied extensively over the past three decades. Current models, as reviewed by Jo and Harris in this issue, hold that the vasopressin induced changes in water permeability are due to the insertion and retrieval of "water channel" proteins to and from the apical membrane of collecting duct cells. There is now abundant functional and morphological evidence supporting the presence of water channels in the apical membrane of collecting duct. Following the discovery of AQP CHIP as the first identified water channel protein [4, 5], which is present in many water transporting tissues including the kidney proximal tubules and thin descending limb of Henle [6 we succeeded in cloning another water channel, AQP which is expressed in collecting ducts [9]. Accumulating evidence indicates that AQP is the vasopressin regulated water channel of collecting duct. 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