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 (Vm), intracellular pH (pHi), intracellular sodium activity (αNai) and intracellular chloride activity (αCli), were recorded during selected disturbances of peritubular fluid composition. The following results were obtained, (a) A sudden decrease of [HCO3]0 leads to Vm depolarization, intracellular acidification and decrease of αNai. (b) A rapid fall of [Na]0 elicits Vm depolarization and decreases pHi; 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 αCli. (d) In the functional absence of CO2/ HCO3 buffer (nominally CO2-free solution plus methazolamide), the reduction of [Na]0 has no effect on Vm and/or pHi. We conclude that the distal tubule basolateral cell membrane is endowed with an electrogenic chlorid-eindependent 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.