Assessment of collecting tubule hydrogen ion secretion in acute respiratory alkalosis using the urinary pCO2

Abstract

The use of the urine-blood (U-B) pCO2 difference as a marker of collecting tubule H+ secretion (CTH+S) faces serious interpretative pitfalls when applied to animals with respiratory acidosis. The present study was aimed to examine the use of this parameter in rats with acute respiratory alkalosis. During infusion of sodium bicarbonate, the U-B pCO2 was only slightly lower in hypocapnic than in eucapnic rats (30±2.2 and 39±3.3 mmHg,p<0.05) and this difference was no longer significant when this parameter was examined as a function of urine bicarbonate concentration. In contrast, the increment in urine pCO2 elicited by bicarbonate loading (i.e. the Δ pCO2) was markedly reduced in hypocapnic as compared to eucapnic rats (22±3.0 and 38±4.5 mmHg, respectively, p<0.01). The infusion of carbonic anhydrase while the urine was highly alkaline and the blood pCO2 kept constant resulted in a decrement in eurine pCO2 which was less in hypocapnic than in eucapnic rats (−23.9±1.9 vs −33±2.8 mmHg, p<0.02). These findings indicate that pCO2 generation from CTH+S and titration of bicarbonate is reduced in hypocapnic rats. The data are in accord with our proposal that the Δ pCO2 is a better index of CTH+S than the U-B pCO2 in the assessment of respiratory acid-base disorders.