Purinergic modulation of Na+,K+,Cl- cotransport and MAP kinases is limitedto C11-MDCK cells resembling intercalated cells from collecting ducts

We demonstrated recently that in renal epithelial cells from collecting duc ts of Madin-Darby canine kidneys (MDCK), Na+,K+,Cl- cotransport is inhibite d up to 50% by ATP via its interaction with P-2Y purinoceptors (Biochim. Bi ophys. Acta 1998. 1369:733-239). In the present study we examined which typ e of renal epithelial cells possesses the highest sensitivity of Na+,K+,Cl- cotransport to purinergic regulation. We did not observe any effect of ATP on Na+,K+,Cl- cotransport in renal epithelial cells from proximal and dist al tubules, whereas in renal epithelial cells from rabbit and rat collectin g ducts ATP decreased the carrier's activity by similar to 30%. ATP did not affect Na+,K+,Cl- cotransport in C7 subtype MDCK cells possessing the prop erties of principal cells but led to similar to 85% inhibition of this carr ier in C11-MDCK cells in which intercalated cells are highly abundant. Both C7- and CII-MDCK exhibited ATP-induced IF, and cAMP production and transie nt elevation of [Ca2+](i). In contrast to the above-listed signaling system s, ATP-induced phosphorylation of ERK and JNK MAP kinases was observed in C 11-MDCK only. Thus, our results reveal that regulation of renal Na+,K+,Cl- cotransport by P-2Y receptors is limited to intercalated cells from collect ing ducts and indicate the involvement of the MAP kinase cascade in puriner gic control of this ion carrier's activity.