Abstract
Diamox, administered during experimental chronic respiratory acidosis in an amount sufficient to inhibit completely renal carbonic anhydrase, resulted in marked increase in plasma pCO2 and bicarbonate concentration. Inhibition of red blood cell carbonic anhydrase was probably responsible for the very high plasma pCO2 observed. The high pCO2, in turn, was capable of so accelerating the uncatalyzed formation of carbonic acid in the renal tubular cell that sufficient secretion of hydrogen ion occurred to accomplish reabsorption of even increased amounts of filtered bicarbonate in the face of complete inhibition of renal carbonic anhydrase. Despite accelerated bicarbonate reabsorption, hyperchloremia and potassium deficiency supervened in blood, ammonia excretion increased, and renal glutaminase was activated.
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