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Pitts, Lotspeich, Ayer, and Schiess (1, 2) have shown that in acute metabolic acidosis or alkalosis the normal kidney handles bicarbonate as if there were a maximal rate of tubular reabsorption which is a direct linear function of the glomerular filtration rate (approximately 2.5 to 2.8 mEq. HCO5 per 100 cc. GFR, in dog and man). At plasma bicarbonate concentrations significantly below 25 mEq. per L., bicarbonate is completely reabsorbed and the urine is acid. When plasma bicarbonate concentration is elevated above this threshold value all the filtered bicarbonate in excess of the limiting rate is excreted in the urine. In respiratory disturbances of acid-base balance, however, the bicarbonate threshold must be changed considerably, because in respiratory alkalosis the urine is alkaline despite low plasma bicarbonate concentrations (3-5) and in respiratory acidosis it is acid when plasma bicarbonate is high (6). The mechanisms initiating these changes in bicarbonate transport have not yet been elucidated, although from a priori considerations one would suspect that they must operate through a change in either carbon dioxide tension or extracellular fluid pH. The purpose of this report is to present observations demonstrating that respiratory regulation of bicarbonate reabsorption is effected through changes in carbon dioxide tension and is independent of extracellular fluid pH.

THE REGULATION OF RENAL BICARBONATE REABSORPTION BY PLASMA CARBON DIOXIDE TENSION 1