IDENTIFICATION AND PROPERTIES OF PATHWAYS FOR K+ TRANSPORT IN GUINEA-PIG AND RAT ALVEOLAR EPITHELIAL TYPE-II CELLS

1. Rb-86(+) was used to study potassium uptake and efflux in type II pneumocytes freshly isolated from adult guinea-pig and rat lung. 2. Both species exhibited a substantial ouabain-sensitive component of potassium influx. 3. In rats, most of the ouabain-resistant influx was abolished by bumetanide and removal of extracellular chloride elicited no further effect. In contrast, only a proportion of the ouabain-insensitive uptake was inhibitable by bumetanide in guinea-pigs and this species showed an additional component of influx, which was chloride dependent and which was reduced by either the K+-H+-ATPase inhibitor, omeprazole, or by the stilbene derivative, 4,4'-diisothiocyanostilloene-2,2'-disulphonate (DIDS). The chloride-dependent component was also apparent in efflux experiments in guinea-pigs, but was absent in rats. 4. Ouabain-insensitive ATPase activity was assayed in highly purified apical membranes from guinea-pig type II pneumocytes. This activity was inhibitable by omeprazole (apparent inhibition constant, K-i, was similar to 40 mu M), was potassium dependent (apparent activation constant, K-a, was similar to 200 mu M) and was doubled by the addition of nigericin. 5. While potassium transport in rat type II cells is adequately accounted for by Na+-K+-ATPase and Na+-K+-2Cl(-) cotransport, our data suggest the additional presence of K+-Cl- cotransport and K+-H-+-ATPase in guinea-pig type II pneumocytes. A model of how alveolar subphase acidification may occur is proposed.