Regulation of BK-α expression in the distal nephron by aldosterone and urine pH.
Regulation of BK-α expression in the distal nephron by aldosterone and urine pH.
复制标题
醛固酮和尿液 pH 值对远端肾单位 BK-α 表达的调节。
DOI：
10.1152/ajprenal.00171.2013
复制
发表时间：
2013
期刊：
影响因子：
--
通讯作者：
Sansom,StevenC
中科院分区：
文献类型：
--
作者：
Wen,Donghai;Cornelius,RyanJ;Yuan,Yang;Sansom,StevenC
In the distal nephron, the large-conductance Ca-activated K (BK) channel, comprised of a pore-forming-α (BK-α) and the BK-β4 subunit, promotes K excretion when mice are maintained on a high-K alkaline diet (HK-alk). We examined whether BK-β4 and the acid-base status regulate apical membrane expression of BK-α in the cortical (CCD) and medullary collecting ducts (MCD) using immunohistochemical analysis (IHC) and Western blot. With the use of IHC, BK-α of mice on acontrol diet localized mostly cytoplasmically in intercalated cells (IC) of the CCD and in the perinuclear region of both principle cells (PC) and IC of the MCD. HK-alk wild-type mice (WT), but not BK-β4 knockout mice (β4KO), exhibited increased apical BK-α in both the CCD and MCD. When given a high-K acidic diet (HK-Cl), BK-α expression increased but remained cytoplasmic in the CCD and perinuclear in the MCD of both WT and β4KO. Western blot confirmed that total BK-α expression was enhanced by either HK-alk or HK-Cl but only increased in the plasma membrane with HK-alk. Compared with controls, mice drinking NaHCO3water exhibited more apical BK-α and total cellular BK-β4. Spironolactone given to mice on HK-alk significantly reduced K secretion and decreased total cellular BK-α but did not affect cellular BK-β4 and apical BK-α. Experiments with MDCK-C11 cells indicated that BK-β4 stabilizes surface BK-α by inhibiting degradation through a lysosomal pathway. These data suggest that aldosterone mediates a high-K-induced increase in BK-α and urinary alkalinization increases BK-β4 expression, which promotes the apical localization of BK-α.
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DOI：
10.1152/ajprenal.00018.2007
发表时间：
2007-07-01
影响因子：
4.2
作者：
Grimm, P. Richard;Foutz, Ruth M.;Sansom, Steven C.
通讯作者：
Sansom, Steven C.
影响因子：
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作者：
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通讯作者：
MCQUEEN, EG
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DOI：
10.1172/jci113967
发表时间：
1989
期刊：
The Journal of clinical investigation
影响因子：
--
作者：
Sweiry,JH;Binder,HJ
通讯作者：
Binder,HJ
影响因子：
3.4
作者：
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通讯作者：
Hoshi, T
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DOI：
10.1152/ajprenal.1982.242.5.f514
发表时间：
1982
期刊：
The American journal of physiology
影响因子：
--
作者：
Stokes,JB
通讯作者：
Stokes,JB