Direct determination of PCO₂ in the rat renal cortex

The mechanism by which the kidney reabsorbs sodium bicarbonate could be a result of: (a) H⁺ secretion, (b) direct HCO^-₃ reabsorption, or (c) a combination of both processes. Most of the studies which have supported the H⁺ secretory theory have involved the assumption that tubular fluid and arterial PCO₂ were equal. We have utilized a new PCO₂ microelectrode to directly determine in situ PCO₂ of tubular fluid and stellate vessel blood in the cortex of the rat kidney during control conditions and after alterations in acid-base status. In 21 control rats, proximal tubular fluid PCO₂ exceeded systemic arterial PCO₂ (ΔPCO₂) by 25.9 ± 0.92 mm Hg (P < 0.001). The values obtained for both distal tubular fluid and stellate vessel blood were not significantly different from proximal tubular PCO₂. Evaluation of PCO₂ in the proximal tubules of Munich-Wistar rats did not reveal evidence for a declining profile for PCO₂ along the length of the nephron. When proximal bicarbonate reabsorption was increased or decreased acutely by alterations in acid-base status, ΔPCO₂ changed in parallel. Furthermore, benzolamide administration significantly reduced ΔPCO₂. We conclude: (a) that the PCO₂ in tubular fluid is significantly greater than systemic arterial PCO₂ (b) that there is no tendency for the observed PCO₂ to fall along the proximal tubule, (c) the mean PCO₂ in the proximal and distal tubules as well as the stellate vessel is not significantly different, thereby rendering the concept of a 'diffusion barrier' for CO₂ in the proximal tubule unlikely, and (d) the level of renal cortical PCO₂ appears to vary directly with the magnitude of bicarbonate reabsorption.