Dietary sodium depletion with elevated aldosterone levels induces electrogenic, amiloride-sensitive sodium absorption and inhibits electroneutral sodium chloride absorption in the rat distal colon. To assess the role of aldosterone in the production of these changes, unidirectional 22Na and 36Cl fluxes were performed under voltage clamp conditions across isolated distal colonic mucosa of rats given continuous aldosterone infusions for up to 12 days. Aldosterone infusion for 7-12 days produced identical changes in both electrogenic sodium absorption and electroneutral sodium chloride absorption compared with dietary sodium-depleted animals. In contrast, aldosterone at 24, 48, and 72 h produced varying changes in ion transport: electrogenic sodium absorption progressively increased, whereas electroneutral sodium chloride absorption was initially augmented but then inhibited. Aldosterone induced active potassium secretion, demonstrated by a reversed short-circuit current after addition of amiloride, in all experimental groups. These results demonstrate that the changes in ion transport observed in sodium-depleted animals are produced by aldosterone, and that aldosterone not only stimulates electrogenic sodium absorption and potassium secretion but in a time-dependent manner both stimulates and inhibits electroneutral sodium chloride absorption.