Factors affecting proximal tubular acidification of non‐bicarbonate buffer in the rat.

The effect of peritubular PCO2 and pH changes within the physiological range on proximal tubular acidification of non‐bicarbonate (phosphate) buffer was evaluated with and without carbonic anhydrase inhibition by stopped‐flow microperfusion and Sb micro‐electrode techniques. Luminal steady‐state pH was reduced from 6.69 to 6.37 and H ion fluxes (JH+) increased from 0.63 to 1.57 nmol cm‐2 s‐1 by increasing capillary CO2 from 0 to 9.6% at pH 7.2. After acetazolamide a marked, although attenuated, effect of CO2 on acidification was still observed; JH+ increased from 0.088 nmol cm‐2 s‐1 at 0% CO2 to 0.78 at 9.6% CO2. Most of this effect can be explained by titration of luminal buffer by CO2, uncatalysed CO2 hydration and H2CO3 recirculation. An increase in capillary CO2 reduced acidification half‐times (t/2), which, according to an analogue circuit model, may be due to increased H ion access to the pump. Peritubular pH changes at 0% CO2 also modified tubular acidification, increasing JH+ from 0.73 nmol cm‐2 s‐1 at pH 7.6 to 0.99 at pH 7.0. After acetazolamide, JH+ still increased from 0.11 nmol cm‐2 s‐1 at pH 7.6 to 0.57 at pH 7.0. In conclusion, both peritubular CO2 changes at constant pH and pH changes at 0% CO2 were effective to modify JH+, in the presence and absence of carbonic anhydrase activity. In the studied range, capillary CO2 induced larger changes in JH+ than pH. The data show substrate (H ion) is a limiting factor for tubular H ion secretion.