FUNCTIONAL ADAPTATION TO HIGH PCO2 OF APICALLY AND BASOLATERALLY LOCATED NA+ H+ EXCHANGE ACTIVITIES IN CULTURED RENAL-CELL LINES/

Cultured renal epithelial cells grown on filter support were examined for functional adaptation of Na+/H+ exchange activities to ''respirato ry'' acidaemia, which was mimicked by increasing PCO2 from 5% to 10% d uring 24 h or 48 h of cell culture. We have selected proximal tubular cell lines with. either dual location of Na+/H+ exchange activities (M CT cells, RKPC-2 cells), apical location of Na+/H+ exchange activity ( OK/WOK cells) or a basolateral location of Na+/H+ exchange activities (LLC-PK1/clone 4 cells, MDCK cells). Na+/H+ exchange activity was dete rmined microspectrofluorometrically (using BCECF) in the absence of CO 2/HCO3-. Respiratory acidaemia specifically increased apical Na+/H+ ex change activity (previously classified as amiloride-resistant) in MCT cells, in RKPC-2 cells and in WOK cells; it stimulated basolateral Na/H+ exchange activity (previously shown to be amiloride-sensitive) in RKPC-2 cells, in LLC-PK,/clone 4 cells and in MDCK cells, but did not affect basolateral Na+/H+ exchange activity in MCT cells. In MCT and i n RKPC-2 cells the effect of high PCO2 on apical Na+/H+ exchange was p revented by inhibition of protein kinase C. In RKPC-2 cells, activatio n of basolateral Na+/H+ exchange by high PCO2 occurred also when prote in kinase C was inhibited. In conclusion, these studies demonstrate st imulation of apical Na+/H+ exchange, but differential regulation of ba solateral Na+/H+ exchange activities in response to a high-PCO2-induce d acid environment. Protein kinase C activation might be involved in m ediating the effect of acidaemia on stimulation of apical Na+/H+ excha nge activity (MCT and RKPC-2 cells).