Abstract

SummaryPyridoxine deficiency was induced in rats by feeding a diet deficient in pyridoxine. Control rats were pair-fed to the intake of the experimental group. Pyridoxine deficiency was demonstrated in the experimental group by increased xanthurenic acid excretion following a tryptophane load and by development of hypertension. Renal concentrating ability, measured as maximum urinary osmolality following dehydration and vasopressin administration, was impaired in both pyridoxine deficient and control rats. Since both groups were protein depleted as a result of the pair-feeding, urea was given to both groups and renal concentrating ability remeasured. The control group now had normal concentrating ability, whereas the maximum urinary osmolality of the pyridoxine deficient rats was significantly reduced. These results suggest that pyridoxine or some aspect of its metabolism is essential for normal renal concentrating ability.

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