The transport of sulfate was studied in basolateral membrane (BLM) vesicles isolated from rat kidney cortex by centrifugation on a Percoll self-generating gradient. In contrast to sulfate transport at the luminal membrane, sulfate uptake by BLM vesicles was not sodium dependent. However, imposition of an inside greater than outside bicarbonate gradient stimulated BLM sulfate uptake nearly 10-fold and produced a transient overshoot of about 4-fold. This process appeared to become saturated at high concentrations of either bicarbonate or sulfate. Sulfate itself, thiosulfate, and hydroxyl, but not chloride or thiocyanate, were able to substitute for bicarbonate. None of these anions was as effective as bicarbonate. The sulfate/bicarbonate exchange was unaltered by manipulation of membrane potential, suggesting that it was electroneutral. Both bicarbonate stimulation and overshoot could be prevented by known inhibitors of anion transport, including mercuric chloride, 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid, and phloretin. Bicarbonate-stimulated sulfate uptake also was inhibited by thiosulfate, probenecid, and acetazolamide. Thus, rat kidney BLM vesicles showed carrier-mediated anion exchange. Its properties indicate that this carrier may participate in both reabsorptive and secretory sulfate transport.