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BK‐beta4 increases apical BK‐alpha expression in collecting duct intercalated cells (IC)
Author(s) -
Wen Donghai,
Cornelius Ryan,
Hatcher Lori,
Sansom Steven
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.912.12
Subject(s) - bk channel , chemistry , microbiology and biotechnology , endocrinology , medicine , calcium , biology , organic chemistry
The calcium‐activated potassium channel (BK) is comprised of a pore‐forming alpha (BK‐a) and ancillary beta 4 subunit (BK‐b4) in the collecting duct where it has a role to promote urinary K excretion when mice are maintained on a high K, alkaline diet (HK‐alk). We previously showed that both BK‐a and BK‐b4 are up‐regulated in the kidneys of mice on HK‐alk, but not HK‐acid diet. Here we examined the role of BK‐b4 in the regulation of apical BK‐b expression. Immunofluorescence with anti‐BK‐a showed that BK‐a localized mostly in the cytoplasm of intercalated cells (IC) in the mouse cortical collecting ducts (CCD) and was perinuclear in both principle cells (PC) and IC of medullary collecting ducts (MCD). Using anti‐V‐ATPase as a marker for IC subtypes, we found that wild type mice (WT) fed HK‐alk exhibited increased BK‐a expression at the apical membrane of a‐IC, b‐IC, and non‐A, non‐B IC of the CCD and MCD; however, no significant change in the localization of BK‐a was found in WT on HK‐acid. BK‐b4 knock‐out mice (b4‐KO) did not exhibit apical BK‐a expression when consuming HK‐alk. When WT mice on HK‐alk were treated with spironolactone (aldosterone inhibitor) the apical BK‐a expression in the CCD and MCD was significantly reduced. These data suggest that aldosterone mediates the HK‐alk‐induced increase in expression of BK‐b4, which helps trafficking of BK‐b to the apical membrane, thereby promoting urinary K excretion.