K+ depletion increases HCO3- reabsorption in OMCD by activation of colonic H (+) -K (+) -ATPase
Nakamura, S.; Wang, Z.; Galla, J.H.; Soleimani, M.
American Journal of Physiology 274(4): F687-F692
1998
ISSN/ISBN: 0002-9513 PMID: 9575892 Document Number: 494449
To probe the role of the isoforms of H+-K+-ATPase (HKA) in potassium depletion (KD), rats were placed on a KD diet for 2 wk. Colonic HKA (cHKA) mRNA levels increased apprx30-fold in outer medulla, and net HCO3- flux (JtCO2) in outer medullary collecting duct (OMCD) increased (13.1 pmolcntdotmin-1cntdotmm tubule length-1 in control to 17.7 pmolcntdotmin-1cntdotmm tubule length-1 in KD; P<0.01). In normal rats, 1 mM ouabain in perfusate had no effect on JtCO2, whereas 10 muM Sch-28080 decreased JtCO2, to 5.1 pmolcntdot min-1 cntdot mm tubule length-1 (P < 0.001). In KD rats, ouabain 1 mM decreased JtCO2 to 6.3 pmol cntdot min-1 cntdot mm tubule length-1 (P < 0.001). Although 10 muM Sch-28080 also decreased JtCO2 to 4.6 pmolcntdotmin-1cntdotmm tubule length-1 (P< 0.001), the inhibitory effects of Sch-28080 and ouabain were not additive. Removal of K+ from perfusate blocked Sch-28080-sensitive JtCO2 both normal and KD tubules. The data suggest that, in KD, cHKA is induced and mediates increased HCO3- reabsorption in OMCD, cHKA in vivo is sensitive to both Sch-28080 and ouabain, and cHKA activity is dominant.