H+ transport by the aldosterone-deficient rat distal nephron.

The effect of aldosterone on distal nephron acidification was investigated by comparing isolated perfused kidneys from adrenalectomized rats treated for 3 to 5 days with dexamethasone alone (10 micrograms/day i.p.) and from rats given in addition a physiologic dose of d-aldosterone (10 micrograms/day in oil s.c.). The maximal pH gradient between urine and perfusate, determined at a perfusate pH of 6.7 with glucose as the sole substrate, did not differ significantly between the aldosterone deplete and replete groups (1.27 +/- 0.12 vs. 1.35 +/- 0.12). H+ secretory capacity of the distal nephron was determined by perfusing kidneys at pH 6.8 and providing saturating quantities of urinary buffer in the form of creatinine. Under these experimental conditions kidneys from aldosterone deplete rats had a higher urine pH and lower excretion rate of titratable acid indicative of a defect in H+ secretion. Acid secretion below a pH of 6.0 (T.A.-pH 6.0), an index of H+ secretion by the distal nephron, was also significantly lower in the aldosterone deplete kidneys. Thus, aldosterone depletion decreased the H+ secretory capacity of the distal nephron, but had no clear effect on the force of the pump as reflected by the maximal pH gradient. Amiloride (10(-5) M) was added to the perfusate of kidneys undergoing the H+ secretory capacity protocol to distinguish between sodium-linked and sodium-independent effects of aldosterone. The difference in T.A. pH 6.0 between aldosterone deplete and replete kidneys was reduced by approximately 70% in the presence of amiloride. This indicates that a substantial portion of the aldosterone-dependent component of distal nephron H+ secretion is mediated by a sodium-dependent mechanism.