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

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.