Oxalate transport across the contraluminal membrane of the proximal tubule was studied in vivo using the "capillary stopped flow microperfusion method" (Pflügers Arch 400:250-256, 1984). Cellular uptake of oxalate was characteristic of a carrier-mediated transport process (Jmax = 1.6 +/- 0.6 pmol/s per cm proximal tubular length, Km = 2.03 +/- 0.77 mmol/l). Sulphate inhibited oxalate transport in a dose-dependent manner (Ki-value = 1.53 +/- 0.38 mmol/l). Sulphate transport across the basolateral membrane was also characteristic of a carrier- mediated transport process (Jmax = 1.83 +/- 0.56 pmol/s per cm proximal tubular length, Km = 1.37 +/- 0.57 mmol/l). Oxalate inhibited the sulphate transport in a dose-dependent manner (Ki = 2. 06 +/- 0.82 mmol/l). No significant differences were found between the Ki values and the Km values of the two substances, indicating that oxalate and sulphate are transported by the same carrier across the basolateral membrane of the proximal tubule. Oxalate transport was not dependent on the extracellular sodium or potassium concentration. Bicarbonate competitively inhibited the oxalate transport. Chloride significantly inhibited the oxalate transport, but not dose dependently. It is, therefore, suggested that oxalate is transported into the cell of the proximal tubule in exchange for sulphate or bicarbonate. The dose-independent inhibition by chloride is suggested to be mediated by the coupling of the sulphate (bicarbonate)/oxalate exchanger with the chloride/bicarbonate exchanger at the basolateral membrane of the proximal tubule. This, furthermore, suggests that the transport of oxalate or sulphate across the basolateral membrane might be indirectly coupled with the reabsorption of chloride at this membrane side.