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The ability of the kidney to conserve or excrete free water independent of changes in solute excretion was a prerequisite for the successful adaptation of vertebrates to prolonged periods on land (1, 2). Renal conservation of water in amphibia, reptiles, birds, and mammals is controlled by antidiuretic hormone (ADH)."2 In these animals, body fluid osmolality is maintained within very narrow limits. Whenbody fluid osmolality decreases, ADHlevels fall, causing the excretion of free water via a hypotonic urine. In contrast, when body fluid osmolality rises, ADHis released, stimulating free water retention and excretion of a hypertonic urine. ADHcontrols renal water retention by inserting water channels into the normally watertight apical membranes of the collecting duct. This in turn allows water flow from the tubule lumen along osmotic gradients between the tubular fluid and the surrounding interstitium (2). In addition, ADHenhances sodium reabsorption by the collecting duct (2) and, in some animals, increases transepithelial solute transport in the medullary thick ascending limb, thereby increasing osmotic gradients for water reabsorption. In certain amphibia, dilute urine is stored in a large bladder where it can be reabsorbed in response to ADHsecreted when the body fluid osmolality rises (1). Since ADH-responsive properties of toad urinary bladder granular epithelial cells resemble closely those of principal cells of the mammalian collecting duct, the toad bladder is a useful model of ADH-responsive renal epithelia. In this review, we will discuss our current understanding of the cellular biology and molecular structure of the ADHwater

Current understanding of the cellular biology and molecular structure of the antidiuretic hormone-stimulated water transport pathway.