title: Activation of H(+)-K(+)-ATPase by CO(2) requires a basolateral Ba(2+)-sensitive pathway during K restriction.
abstract: We studied the activation of H(+)-K(+)-ATPase by CO(2) in the renal cortical collecting duct (CCD) of K-restricted animals. Exposure of microperfused CCD to 10% CO(2) increased net total CO(2) flux (J(t CO(2))) from 4.9 +/- 2.1 to 14.7 +/- 4 pmol. mm(-1). min(-1) (P < 0. 05), and this effect was blocked by luminal application of the H(+)-K(+)-ATPase inhibitor Sch-28080. In the presence of luminal Ba, a K channel blocker, exposure to CO(2) still stimulated J(t CO(2)) from 6.0 +/- 1.0 to 16.8 +/- 2.8 pmol. mm(-1). min(-1) (P < 0.01), but peritubular application of Ba inhibited the stimulation. CO(2) substantially increased (86)Rb efflux (a K tracer marker) from 93.1 +/- 23.8 to 249 +/- 60.2 nm/s (P < 0.05). These observations suggest that during K restriction 1) the enhanced H(+)-K(+)-ATPase-mediated acidification after exposure to CO(2) is dependent on a basolateral Ba-sensitive mechanism, which is different from the response of rabbits fed a normal-K diet, where activation of the H(+)-K(+)-ATPase by exposure to CO(2) is dependent on an apical Ba-sensitive pathway; and 2) K/Rb absorption via the apical H(+)-K(+)-ATPase exits through a basolateral Ba-sensitive pathway. Together, these data are consistent with the hypothesis of cooperation between H(+)-K(+)-ATPase-mediated acidification and K exit pathways in the CCD that regulate K homeostasis.
authors.affiliation: Laboratory of Epithelial Transport, Division of Nephrology, Hypertension, and Transplantation, Department of Medicine, University of Florida, and Nephrology Section, Veterans Affairs Medical Center, Gainesville, Florida 32608-1197, USA.
authors.forename: X
authors.initials: X
authors.lastname: Zhou
authors.forename: I J
authors.initials: IJ
authors.lastname: Lynch
authors.forename: S L
authors.initials: SL
authors.lastname: Xia
authors.forename: C S
authors.initials: CS
authors.lastname: Wingo
mesh_terms: D000818:Animals; D001464:Barium / Q000494:pharmacology*; D001692:Biological Transport / Q000187:drug effects; D002245:Carbon Dioxide / Q000494:pharmacology*; D016764:Cell Polarity; D004789:Enzyme Activation / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D017506:H(+)-K(+)-Exchanging ATPase / Q000378:metabolism*; D007093:Imidazoles / Q000494:pharmacology; D066298:In Vitro Techniques; D007685:Kidney Tubules, Collecting / Q000187:drug effects* / Q000201:enzymology* / Q000378:metabolism; D008954:Models, Biological; D011188:Potassium / Q000008:administration & dosage / Q000378:metabolism* / Q000494:pharmacology; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000378:metabolism; D054328:Proton Pump Inhibitors; D011817:Rabbits; D012413:Rubidium / Q000378:metabolism
chemical_list: D004791:Enzyme Inhibitors; D007093:Imidazoles; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D054328:Proton Pump Inhibitors; C035235:Sch 28080; D002245:Carbon Dioxide; D001464:Barium; D017506:H(+)-K(+)-Exchanging ATPase; D012413:Rubidium; D011188:Potassium