Experiments in dome epithelium of Madin-Darby canine kidney (MDCK) cells were performed to elucidate aldosterone action on acid-base transport. By means of pH-sensitive microelectrodes the pH of the dome fluid was measured while the apical plasma membrane was superfused. In the absence of HCO3- the dome fluid (facing the basolateral cell membrane) alkalinized in response to 10(-7) mol/l aldosterone. Amiloride (10(-3) mol/l) inhibited dome formation and pH recovery of the dome fluid from an extracellular acid load. In the presence of HCO3- dome fluid acidified in response to aldosterone. The stilbene derivative diisothiocyanate-stilbene-2,2'-disulphonic acid (DIDS) or removal of Cl- from the apical perfusate inhibited this dome acidification. In aldosterone-depleted MDCK monolayers HCO3- was actively accumulated in the dome fluid in contrast to aldosterone-supplemented cells. The results indicate that aldosterone stimulates both amiloride-sensitive Na+/H+ exchange and DIDS-sensitive Cl-/HCO3- exchange in the apical cell membrane of MDCK cells. In the absence of aldosterone the HCO3- extrusion process is localized in the basolateral membrane in series with apical Na+/H+ exchange, while in the presence of aldosterone Cl-/HCO3- is mainly localized in the apical membrane in parallel with Na+/H+ exchange. Cl- exits the cell through apical Cl- channels and is absorbed via the paracellular route.