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In man, dog, and rat the induction of metabolic acidosis leads to an increase in renal production and excretion of ammonia (2-4) that appears to derive primarily from glutamine (4-6). Studies of the renal cortex of the acidotic rat reveal an increase in the activity of glutaminase I, the enzyme that deamidates glutamine to glutamate (Figure 1), and it is assumed that this may contribute to the increase in ammoniagenesis from glutamine (2). The mechanism by which acidosis evokes an increase in renal glutaminase I activity in the rat is not known. If acidosis directly stimulates the synthesis or activation of glutaminase I it would be expected that the intracellular concentration of glutamate would be increased. Actually, the glutamate content of the renal cortex of acidotic rats is decreased (7, 8). The concurrence in acidotic rats of decreased renal glutamate concentration and increased renal glutaminase I activity is of much interest. In a variety of biologic systems there exists a negative feedback between the intracellular concentration of an immediate or distant product of an enzymatic

Renal gluconeogenesis in acidosis, alkalosis, and potassium deficiency: its possible role in regulation of renal ammonia production.