TITLE:
Potassium Depletion Stimulates Beta-Subunit of Colonic H+-K+-ATPase in Mice
AUTHORS:
Guojun Wei, James J. Ravellette, Suguru Nakamura
KEYWORDS:
H+-K+-ATPase (HKA); Knockout Mice (KO); Wild-Type Mice (WT); Gastric H+-K+-ATPase (gHKA); Colonic H+-K+-ATPase (cHKA); Outer Medullary Collecting Duct (OMCD)
JOURNAL NAME:
International Journal of Clinical Medicine,
Vol.4 No.5,
May
16,
2013
ABSTRACT: H+-K+-ATPase
(HKA) is composed of two different subunits: an alpha and a beta subunit. Previous studies have shown that in the kidney gastric
HKA (HKA alpha 1) predominates under normal dietary conditions while colonic HKA
(HKA alpha 2) predominates under potassium depleted conditions [1]. The purpose
of the current study was to elucidate the association between the beta and different
alpha subunits from stomach, colon and kidney under normal and potassium
depleted conditions. Black Swiss mice were fed a potassium-free diet for 2
weeks, beta subunit expression of HKA in stomach mucosae, colon mucosae and
renal outer medulla was examined and compared between normal diet and potassium depleted diet. In wild type (WT) mice, the
concentrations of the beta subunit under potassium deficient conditions were
found significantly increased compared with normal dietary conditions in colon
mucosae (8.27 ± 0.73 vs 6.62 ± 0.55 μg/μl, n = 7, p = 0.0416), whereas in cHKA (HKA alpha 2) mice colon
mucosae, the concentrations of the beta subunit were statistically the same
(5.05 ± 0.31 vs 4.76 ± 0.37 μg/μl, n = 13, p = 0.2833), and the concentration of the beta subunit
stayed the same in renal outer medulla and stomach mucosae as well. The data
indicate that potassium deficiency results in a
significant increase in the levels of HKA beta subunit concentration in the
colonic tissue of WT mice. The results indicate that the HKA beta subunit
associates with the cHKA (HKA alpha 2) in order to mediate bicarbonate reabsorption under potassium depletion (hypokalemia)