POTASSIUM SECRETION IS INHIBITED BY METABOLIC-ACIDOSIS IN RABBIT CORTICAL COLLECTING DUCTS IN-VITRO

The role of metabolic acidosis in the regulation of transepithelial po tassium transport was examined in rabbit cortical collecting ducts (CC D) using in vitro isolated tubular microperfusion and conventional mic roelectrode techniques. Basolateral metabolic acidosis, created by red uction of bicarbonate concentration from 25 to 5 meq/l, pH 7.40 to 6.8 0, depolarized the transepithelial voltage significantly (-6.5 +/- 1.0 to -2.7 +/- 1.3 mV). Basolateral acidosis also suppressed net potassi um secretion(-14.3 +/- 2.1 to -9.0 +/- 1.7 pmol min(-1).mm(-1)). Elect rophysiological study in CCD cells demonstrated that basolateral metab olic acidosis depolarized transepithelial voltage and apical and basol ateral membrane voltage with an increase of transepithelial and fracti onal apical resistance. Basolateral acidosis did not affect the Na-22 efflux nor Rb-86 efflux. The inhibitory action of basolateral acidosis on net potassium secretion remained in the presence of luminal barium and in the absence of bicarbonate. Ouabain could not abolish the effe ct of basolateral acidosis on transepithelial voltage completely. Thes e data lead us to conclude that basolateral acidosis affects multiple transport pathways, and it inhibits mainly apical barium-sensitive pot assium transport. Additionally, it inhibits apical sodium conductance, barium-insensitive potassium transport, and stimulates a ouabain-inse nsitive electrogenic transport pathway to some degree.