Potassium Depletion Stimulates Beta-Subunit of Colonic H+-K+-ATPase in Mice

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)