Failure of increased sodium avidity to facilitate renal acid excretion in dogs fed sulfuric acid

Abstract

Previous studies have suggested that the increment in renal acid excretion caused by sulfuric acid feeding is mediated solely by an interplay between the sulfate-induced increase in distal sodium delivery and the gradual augmentation of distal sodium reabsorption that occurs as sodium losses accumulate. This hypothesis predicts that if distal sodium reabsorption were stimulated sufficiently prior to the administration of sulfuric acid, excretion of the hydrogen ion load would occur promptly, thus obviating the fall in plasma bicarbonate or loss of cation that normally occurs. To test this prediction, we fed sulfuric acid (7 mEq of H+/kg/day) to dogs in which distal sodium avidity had been enhanced prior to acid feeding either by diuretic-induced sodium depletion (N = 6) or by deoxycorticosterone acetate 7.5 mg, twice a day and a low-sodium diet (N = 8). Contrary to expectation, over the first 3 days of acid feeding there was a significant fall in plasma bicarbonate (7.1 and 7.5 mEq/liter) and an increase in urinary sodium excretion (48 mEq in both groups). Moreover, changes in both plasma bicarbonate and urinary sodium excretion were similar to those observed previously (5.9 mEq/liter and 46 mEq, respectively) in normal dogs fed the same dose of sulfuric acid.