BASOLATERAL ELECTROGENIC NA/HCO3 SYMPORT IN THE AMPHIBIAN DISTAL TUBULE

This study was carried out to assess whether the amphibian distal tubule possesses a basolateral Na/(HCO3)n > 1 cotransport. The experiments were performed in the kidney of Necturus maculosus in vivo, by means of double-barreled selective microelectrodes. Basolateral membrane potential (V(m)), intracellular pH (pH(i)), intracellular sodium activity (alpha-Na(i)) and intracellular chloride activity (alpha-Cl(i)) were recorded during selected disturbances of peritubular fluid composition. The following results were obtained. (a) A sudden decrease of [HCO3]o leads to V(m) depolarization, intracellular acidification and decrease of alpha-Na(i). (b) A rapid fall of [Na]o elicits V(m) depolarization and decreases pH(i); these patterns are not substantially altered in the presence of millimolar amiloride concentrations or in the nominal absence of peritubular Cl. (c) An acute decrease of [Na]o does not alter alpha-Cl(i). (d) In the functional absence of CO2/HCO3 buffer (nominally CO2-free solution plus methazolamide), the reduction of [Na]o has no effect on V(m) and/or pH(i). We conclude that the distal tubule basolateral cell membrane is endowed with an electrogenic chloride-independent Na/base carrier, mediating Na and base efflux. The blockade of this carrier by carbonic anhydrase inhibitor indicates that the cotransported base is HCO3 or a related species.