Conventional microelectrodes were used to examine the electrogenic pathways for bicarbonate transport across the basolateral membranes of proximal convoluted (PCT) and straight (PST) tubule segments of the rabbit kidney perfused in vitro. When bath bicarbonate concentration was reduced from 22 to 6.6 mM at a constant pH, transient depolarizations lasting several seconds with a peak value of approximately 15 mV were seen in both tubule segments. Acetazolamide (0.1 mM) in the lumen and bath solutions reduced the magnitude and increased the duration fo this response. The final pH of the bathing solution influenced both the peak height and steady-state values of the intracellular potential when bicarbonate concentration was reduced either with constant CO2 or with an increase in CO2. Reducing bath sodium concentration by replacement with either tetramethylammonium or N-methyl-D-glucamine resulted in a sustained depolarization of both PCT and PST cells. This response was inhibited by the addition of 10(-4) M 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonate (SITS) in the bathing solution. By analogy with bicarbonate transport in rat and amphibian proximal tubules, these data suggest that bicarbonate exit across the basolateral membrane of the rabbit proximal tubule is electrogenic and coupled to sodium and that basolateral bicarbonate exit can be inhibited by both acetazolamide and SITS in the bathing solution.