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 coll ecting 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 lum inal application of the H+-K+-ATPase inhibitor Sch-28080. In the presence o f 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 peritubular application of Ba inhibited the stimulation. CO2 substantially increased Rb-86 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; a nd 2) K/Rb absorption via the apical H+-K+-ATPase exits through a basolater al Ba-sensitive pathway. Together, these data are consistent with the hypot hesis of cooperation between H+K+-ATPase- mediated acidification and K exit pathways in the CCD that regulate K homeostasis.