The effects of Aldosterone on the intracellular pH recovery rate (pHirr) via Na⁺/H⁺ exchanger and on the [Ca²⁺]i were investigated in isolated rat S3 segment. Aldosterone [10^-12, 10^-10 or 10^-8 M with 1 h, 15 or 2 min preincubation (pi)] caused a dose dependent increase in the pHirr, but Aldosterone (10^-6 M with 1 h, 15 or 2 min pi) decreased it (these effects were prevented by HOE694 but not by S3226). After 1 min of Aldosterone pi there was a transient and dose-dependent increase of the [Ca²⁺]i and after 6 min pi there was a new increase of [Ca²⁺]i that persisted after 1h. Spironolactone, Actinomycin D or Cycloheximide did not affect the effects of Aldosterone (15 or 2 min pi), but inhibited the effects of Aldosterone (1 h pi) on pHirr and on [Ca²⁺]i. RU 486 prevented the stimulatory effect of Aldosterone (10^-12 M, 15 or 2 min pi) on both parameters and maintained the inhibitory effect of Aldosterone (10^-6 M, 15 or 2 min pi) on the pHirr but reversed its stimulatory effect on the [Ca²⁺]i to an inhibitory effect. The data indicate a genomic (1h, via MR) and a nongenomic action (15 or 2 min, probably via GR) on [Ca²⁺]i and on the basolateral NHE1 and are compatible with stimulation of the NHE1 by increases in [Ca²⁺]i in the lower range (at 10^-12 M Aldosterone) and inhibition by increases at high levels (at 10-6 M Aldosterone) or decreases in [Ca²⁺]i (at 10-6 M Aldosterone plus RU 486).