THE ROLE OF PLASMA CO2 TENSION AND CARBONIC ANHYDRASE ACTIVITY IN THE RENAL REABSORPTION OF BICARBONATE*

Abstract

The effect of plasma pCO2 on maximal HCO3-reabsorptive capacity (HCO3-Tm) was assessed in 15 dogs before and after inhibition of carbonic anhydrase. Bicarbonate reabsorption increased curvilinearly as plasma pCO2 was elevated. Inhibition of carbonic anhydrase depressed the HCC3-Tm by a constant amount at all CO2 tensions. In a 2d group of experiments the effects of variations in plasma PCO2 and inhibition of carbonic anhydrase on the excretion of HCO3- as the HCO3-Tm was approached were studied in 15 dogs. When plasma pCO2 was maintained constant at a normal level, HCO3" excretion began before the Tm was reached. A similar leak was noted in respiratory acidosis. Carbonic anhydrase inhibition, however, caused a HCO3-leak which was of greater magnitude and which occurred even at very low concentrations of plasma HCO3". Increasing H+ production by elevating plasma pCO2 to 110 to 130 mm Hg failed to obliterate the HCO3-leak. It was concluded that HCO3 -reabsorption was accomplished by 2 distinct processes. One process, presumably located in the proximal tubule, has a HC03-Tm which is dependent upon plasma CO2 tension and independent of carbonic anhydrase, and a transport system sensitive to the pH of tubular fluid. Carbonic anhydrase, by catalyzing the dehydration of carbonic acid at the luminal surface, prevents drastic lowering of the pH, thereby facilitating HCO3 reabsorption. A 2d process, apparently located in the distal tubule, has a fixed HCO3-Tm which is dependent upon carbonic anhydrase, independent of changes in plasma pCO2 and can operate efficiently despite sharp pH gradients.