Abstract
Na+, K+, NH4+, urea, and water content were measured in the renal cortex, medulla, and papilla of normal rats and of rats with hereditary hypothalamic diabetes inslpidus (DI) under various experimental conditions. The medullary and papillary contents of Na (m[image]/100 g dry solids) were no greater in normal rats than in DI rats drinking ad libitum. Nor were these contents increased in DI rats after they had been treated for 3 days with large amounts of vasopressin. In contrast, the medullary and papillary contents of urea were significantly greater in normal animals and DI rats treated with vasopressin than in untreated DI animals. These results suggest that vasopressin does not decrease medullary blood flow below normal or enhance the reabsorption of Na from the loops of Henle. All the data can be explained through a sole action of vasopressin that alters the permeability to water and urea of membranes lining the tubules of the distal nephron. The medullary and papillary contents of both Na and urea were higher in normal rats deprived of drinking water for 48 hr. than in normal rats drinking ad libitum, but the increases were of undoubted statistical significance only for urea. It is suggested that the composition of the renal medulla and papilla during thirsting depends much more on the extent of dehydration and the possibly consequent effects on glomerular filtration rate (GRF) and medullary blood flow than on changes in the concentration of endogenous vasopressin. Differences in both degree of hydration and degree of dehydration may largely account for the discrepant results from various laboratories concerning the composition of renal tissues in various states of diuresis and antidiuresis. Twelve hours of dehydration was as effective in raising the medullary and papilllary osmolalities of DI rats as were 3 daily injections of vasopressin. In thirsted DI rats the medullary and papillary contents of Na were not significantly different from those of DI rats drinking ad libitum, but the contents of urea were significantly increased by dehydration. These results emphasize the Importance of mechanisms other than changes in membrane permeability (perhaps principally GFR and medullary blood flow) in the operation of the countercurrent mechanism.

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