Cheval L, Barlet-Bas C, Khadouri C, Feraille E, Marsy S, Doucet A
Laboratoire de Physiologie Cellulaire, Unité de Recherche Associée 219, Centre National de la Recherche Scientifique, Collège de France, Paris.
Am J Physiol. 1991 Jun;260(6 Pt 2):F800-5. doi: 10.1152/ajprenal.1991.260.6.F800.
To evaluate the involvement of K(+)-ATPase activity in K+ transport in the terminal segments of the rat nephron, we searched for the existence of a component of Rb+ uptake into microdissected segments of collecting tubule associated with the activity of this ATPase. Results indicated that K(+)-ATPase is stimulated by K+ and by Rb+ in a similar fashion and that it is specifically inhibited by the imidazopyridine Sch 28080 (apparent affinity approximately 5 x 10(-7) M). In both cortical and outer medullary collecting tubules (CCT and MCT) of normal rats, 10(-4) M Sch 28080 significantly inhibited the initial rate of Rb+ uptake. Sch 28080-sensitive Rb+ uptake in these two nephron segments was not altered by ouabain, as K(+)-ATPase activity. Finally, both K(+)-ATPase activity and Sch 28080-sensitive Rb+ uptake were increased by similar factors in the CCT and MCT of rats fed a K(+)-depleted diet for 3 days. In these two nephron segments, the apparent stoichiometry of K(+)-ATPase was 1 Rb+:1 ATP. These results demonstrate that K(+)-ATPase reflects the activity of a K+ pump that is pharmacologically similar to the gastric H(+)-K+ pump.
