Proximal HCO3- reabsorption and the determinants of tubular and capillary PCO2 in the rat.

Studies were carried out in Munich-Wistar rats to define the CO2 partial pressure (PCO2) profile in the surface tubules and capillaries of the kidney and to relate these measurements to proximal tubular HCO3- reabsorption, renal blood flow, and O2 consumption. In euvolemic rats, PCO2 in Bowman's space (BS) was 12.5 mmHg higher than in arterial blood, indicating CO2 addition to the arterial tree as it traverses the cortex. PCO2 further rose by 3.9 mmHg between the efferent arteriole (EA) and the peritubular capillaries (PC) (P less than 0.01) and by 4.9 mmHg between BS and the early proximal tubule (EP) (P less than 0.01). In studies with paired measurements, PCO2 in EP was 1.8 mmHg higher than in the adjacent PC (P less than 0.05). HCO3- reabsorption in EP (first 0.4-1.25 mm) was 579 pmol X min-1 X mm-1 (34.3 +/- 4.6% of the filtered load). By use of a model of facilitated diffusion of CO2 across the cell, the trans-epithelial PCO2 gradient in EP can be accounted for by the CO2 generated from HCO3- reabsorption, assuming an intracellular pH of 7.3. In the vascular compartment, roughly half the rise in PCO2 between the afferent arteriole (estimated to equal BS PCO2) and PC can be accounted for by metabolic CO2 production and half by titration of blood buffers by reabsorbed HCO3-.