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

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

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


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 (J(t 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 J(t CO2) from 6.0 ± 1.0 to 16.8 ± 2.8 pmol · mm-1 · min-1 (P < 0.01), but pertubular 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.

Original languageEnglish
Pages (from-to)F153-F160
JournalAmerican Journal of Physiology - Renal Physiology
Issue number1 48-1
StatePublished - Jul 2000
Externally publishedYes


  • Acidification
  • Cortical collecting duct
  • Hydrogen-potassium-adenosine 3',5'-triphosphatase
  • Sch-28080


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