Abstract
Infusion of [14C]hypoxanthine into one renal portal circulation of the chicken resulted in an excess of [14C]uric acid excreted into the urine from the infused side kidney. No [14C]hypoxanthine appeared in the urine from either kidney. When the renal metabolism of [14C]hypoxanthine was inhibited by xanthine dehydrogenase inhibitors, almost no excess 14C-label appeared in the urine of the infused side suggesting that formation of nephrogenic urate plays an important role in the tubular excretion of hypoxanthine. A comparison of the effects of inhibitors on the renal excretion of preformed urate and nephrogenic urate suggests the existence of a p-aminohippurate-independent transport step for purines at the luminal membrane of the renal tubular cell. Studies with transport inhibitors suggest that the active transport step is anionic in character.
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