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In the kidney, the initial step in the release of ammonia from glutamine may be catalyzed by either glutaminase or glutarnine ketoacid transaminase systems (4-6, 17). The glutaminase pathway leading to the formation of glutamate, which serves as the intermediate product and may undergo further oxidative deamination to form alpha ketoglutarate and ammonia, appears to be the major one (4). I t has also been reported that glutamate, alpha ketoglutarate, and oxalacetate are among the most effective "feedback" inhibitors of glutaminase activity (3). Therefore, the study of the subcellular organelles .whose function may determine the local concentrations of these metabolites in the renal tubular cells will be helpful in understanding the intracellular structure involved in the formation of ammonia. One important mechanism which may control the cellular concentrations of glutamate and alpha ketoglutarate is the reversible enzymatic transamination reaction between these two dicarboxylic acids. Among the enzymes involved in this reaction, glutamic oxalacetic transaminase (GOT) is the most widely distributed in the mammalian tissues. A previous communication has briefly reported that the activity of this enzyme in the kidney is largely concentrated in the convoluted tubules of the renal cortex and certain cortical tubules near the corticomedullary junction (12). Subsequent work carried out in this laboratory has revealed that the latter are the ascending thick limbs of the loops of Henle. This report is concerned with the relationship of this enzyme activity to the subcellular organdies of these tubular cells, particularly the subapical vesicles. The possible significance of this enzyme to the interrelationship among renal ammonia excretion, gluconeogenesis, and anaerobic carbon dioxide production will be discussed.

THE POSSIBLE ROLE OF THE VESICLES IN RENAL AMMONIA EXCRETION