Regulation of the maximum rate of renal ammoniagenesis in the acidotic dog

Metabolism of glutamine results in the net production of ATP; however, cells cannot sustain an ATP production rate greater than their rate of ATP utilization. The purpose of these studies was to determine whether the rate of ATP turnover in the kidney could set an upper limit on renal glutamine metabolism and thereby renal ammoniagenesis. The acidotic dog kidneys extracted glutamine, lactate, citrate, and oxygen from the arterial blood and added ammonium and alanine to the venous blood. Renal glutamine metabolism was responsible for almost all the ammonium production. Renal ATP production was estimated from the rate of oxygen consumption and appeared to be derived roughly equally from the oxidation of glutamine and lactate. There was no apparent renal glucose production from ATP balance calculations and this impression was supported when the inhibitor of gluconeogenesis, 3-mercaptopicolinate, did not inhibit ammoniagenesis. Approximately 90% of the ATP synthesized was utilized to reabsorb sodium. When the...