Identification and properties of pathways for K+ transport in guinea‐pig and rat alveolar epithelial type II cells.

86Rb+ was used to study potassium uptake and efflux in type II pneumocytes freshly isolated from adult guinea‐pig and rat lung. Both species exhibited a substantial ouabain‐sensitive component of potassium influx. 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'‐diisothiocyanostilbene‐2,2'‐disulphonate (DIDS). The chloride‐dependent component was also apparent in efflux experiments in guinea‐pigs, but was absent in rats. 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, Ki, was approximately 40 microM), was potassium dependent (apparent activation constant, Ka, was approximately 200 microM) and was doubled by the addition of nigericin. 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.