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According to current concepts, renal ammonia synthesis may be attributed to the renal extraction and catabolism of certain plasma amino acids. In 1943, Van Slyke and associates demonstrated in the dog that the amide nitrogen of glutamine was removed from arterial plasma in quantities sufficient to account for approximately 60 per cent of the urinary ammonia excreted during metabolic acidosis (1). It was proposed that the remaining 40 per cent of urinary ammonia could be accounted for by the renal uptake of plasma a-amino nitrogen. In agreement with this hypothesis, many investigators have since shown that the administration of several amino acids other than glutamine is associated with an increased urinary ammonia excretion (2-4). Loading experiments of this type have indicated thatbesides glutamine-glycine, alanine, asparagine, leucine. and histidine may serve as precursors of urine ammonia. The demonstration of appropriate enzyme systems within renal tissue capable of forming ammonia from these substrates has been offered as additional support for the thesis that several plasma amino acids may participate normally in the renal production of ammonia. Nevertheless, the specific amino acids that serve as renal ammonia precursors have not been identified clearly in conditions associated with normal acid-base balance and normal plasma amino acid concentrations. The present study was undertaken for two principal reasons: first, to characterize the' typical patterns of uptake or release

AMINO ACID EXTRACTION AND AMMONIA METABOLISM BY THE HUMAN KIDNEY DURING THE PROLONGED ADMINISTRATION OF AMMONIUM CHLORIDE*