Effect of plasma CO2 tension on renal tubular reabsorption of bicarbonate.

S INCE the extensive studies of Pitts and coworkers (1-3) defined the characteristics of bicarbonate reabsorption in the normal subject, very little additional information has appeared concerning the nature of this transport system or its regulation. It was suggested then (2) that a dual process existed for the reabsorption of bicarbonate. A specific transport system in the proximal tubule was believed to be responsible for the reabsorption of most of the filtered bicarbonate. However, the effective removal of additional bicarbonate and fixed base from distal tubular urine could be accomplished by the same basic mechanism as that responsible for the acidification of the urine, namely by the exchange of H+ in tubular cells with monovalent cation in tubular urine (H+-B+ exchange). The source of H+ for exchange was believed to be the carbonic acid in the tubular cell since it was shown that the inhibition of carbonic anhydrase by sulfanilamide resulted in a decrease in both the titratable acidity of the urine and the reabsorption of bicarbonate. Using the more potent inhibitor, Diamox (‘6063’; 2-acetylaminoI, 3,+thiadiazole-5-sulfonamide), Berliner observed that the amount of additional bicarbonate which appeared in the urine after the inhibition of carbonic anhydrase was far in excess of the IS20% which was believed to escape reabsorption by the proximal tubule. He therefore proposed that the tubular secretion of H+ in exchange for Bf might be the primary mechanism of bicarbonate reabsorption in the proximal as well as the distal tubule (4). --