Altered expression of renal NHE3, TSC, BSC-1, and ENaC subunits in potassium-depleted rats

被引:62
作者
Elkjær, ML
Kwon, TH
Wang, WD
Nielsen, J
Knepper, MA
Frokiær, J
Nielsen, S
机构
[1] Aarhus Univ, Water & Salt Res Ctr, DK-8000 Aarhus C, Denmark
[2] Dongguk Univ, Sch Med, Dept Physiol, Kyungju 780714, South Korea
[3] NHLBI, Kidney & Electrolyte Metab Lab, NIH, Bethesda, MD 20892 USA
关键词
hypokalemia; sodium transport; kidney; urine concentration;
D O I
10.1152/ajprenal.00186.2002
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The purpose of this study was to examine whether hypokalemia is associated with altered abundance of major renal Na+ transporters that may contribute to the development of urinary concentrating defects. We examined the changes in the abundance of the type 3 Na+/H+ exchanger (NHE3), Na+-K+-ATPase, the bumetanide-sensitive Na+-K+-2Cl(-) cotransporter (BSC-1), the thiazide-sensitive Na+-Cl- cotransporter (TSC), and epithelial sodium channel (ENaC) subunits in kidneys of hypokalemic rats. Semiquantitative immunoblotting revealed that the abundance of BSC-1 (57%) and TSC (46%) were profoundly decreased in the inner stripe of the outer medulla (ISOM) and cortex/outer stripe of the outer medulla (OSOM), respectively. These findings were confirmed by immunohistochemistry. Moreover, total kidney abundance of all ENaC subunits was significantly reduced in response to the hypokalemia: alpha-subunit (61%), beta-subunit (41%), and gamma-subunit (60%), and this was confirmed by immunohistochemistry. In contrast, the renal abundance of NHE3 in hypokalemic rats was dramatically increased in cortex/OSOM (736%) and ISOM (210%). Downregulation of BSC-1, TSC, and ENaC may contribute to the urinary concentrating defect, whereas upregulation of NHE3 may be compensatory to prevent urinary Na+ loss and/or to maintain intracellular pH levels.
引用
收藏
页码:F1376 / F1388
页数:13
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