To examine the mechanism by which mineralocorticoids regulate HCO3-absorption in the rabbit inner stripe of the outer medullary collecting duct, we microfluorometrically measured intracellular pH (pH1) in in vitro perfused tubules using 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF) assaying the apical and basolateral membrane H'/OH-/HCO3 (control, 72.7±15.7 pmol -mm-' * min-vs DOCA, 132.3±22.5 pmol. mm-1 min-', P < 0.02), while the K112 for Cl-was unchanged. Basolateral membrane Na+/H+ antiporter activity assayed as the Na+-dependent pH1 recovery from an acid load was not changed in chronic DOCA tubules versus controls. In conclusion, the apical membrane H+ pump and basolateral membrane Cl-/HCO3 exchanger of the rabbit OMCDI are regulated in parallel without chronic alterations in pH1 under the conditions of mineralocorticoid excess and deficiency. The parallel changes in these transporters accounts for the alterations in OMCDj HCO3 absorption seen under these condi-