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Am J Physiol Renal Physiol 279: F153-F160, 2000;
0363-6127/00 $5.00
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Vol. 279, Issue 1, F153-F160, July 2000

Activation of H+-K+-ATPase by CO2 requires a basolateral Ba2+-sensitive pathway during K restriction

Xiaoming Zhou, I. Jeanette Lynch, Shen-Ling Xia, and Charles S. Wingo

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

We studied the activation of H+-K+-ATPase by CO2 in the renal cortical collecting duct (CCD) of K-restricted animals. Exposure of microperfused CCD to 10% CO2 increased net total CO2 flux (Jt CO2) 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 CO2 still stimulated Jt CO2 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. CO2 substantially increased 86Rb 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 CO2 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 CO2 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.

hydrogen-potassium-adenosine 3',5'-triphosphatase; cortical collecting duct; acidification; Sch-28080


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