During antidiuresis, sodium is concentrated in the papilla and medulla of mammalian kidneys as a result of active sodium reabsorption from medullary tubules and countercurrent flow through the loops of Henle and the medullary capillaries. It is clear from chemical (1) and cryoscopic (2, 3) analysis of sections of kidney, and from direct micropuncture (4-6), that under these circumstances the osmolality of medullary interstitial fluid is approximately that of collecting-duct urine and that sodium concentration rises progressively along a gradient from cortex to medulla.The precise role of antidiuretic hormone (ADH) in establishing and maintaining this gradient is not entirely clear, partly because comparable studies in the absence of vasopressin (i.e., during water diuresis) have been more difficult to accomplish. Ullrich, Jarausch and Drenckhahn demonstrated that the osmolality and sodium concentration of papillary water approached that of peripheral plasma in dogs during water diuresis (1, 7). That medullary interstitial fluid is actually hypertonic to plasma in the absence of ADH was suggested by the demonstration (8) that compression of the renal artery of one kidney during water diuresis led to production of hypertonic urine by that kidney. Recently, Bray reported that the

Renal ability to concentrate nonurea solutes in the urine is improved in dogs by feeding protein. This effect is most apparent during osmotic diuresis induced by mannitol and, though partially explicable by increases in GFR, the data suggest that other factors are also involved. The enhanced concentrating ability of protein-fed dogs is probably related to an increased concentration of both sodium and potassium in the renal papilla.

In an attempt to delineate factors responsible for the accumulation of uric acid in renal tissue in vivo, the concentration of urate in renal cortex, medulla and papilla was measured in dogs infused with varying amounts of lithium urate. During antidiuresis, urate concentration increased as the papilla was approached, and with large urate infusions, the concentration of urate in papillary tissue equalled or exceeded that in urine. Renal accumulation of urate was roughly proportional to the plasma level of urate, and was reduced by water loading or mannitol diuresis. Renal concentrating ability was not consistently altered by acute infusions of urate.

The effects of potassium depletion, calciferol-induced hypercalcemia, hyaluronidase, hypercapnia, and adrenal steroids on the water uptake of intact frogs were studied. The findings suggest that potassium depletion and hypercalcemia interfere with water uptake. Hyaluronidase and adrenal glucocorticoids in doses used were without effect on water transport. Water uptake after oxytocin was greatly decreased by exposing frogs to a high concentration of CO2 in air. The data obtained with frog skin in vivo are discussed in relation to in vitro studies with anuran membranes reported by others.

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