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Am J Physiol Renal Physiol 283: F1376-F1388, 2002. First published July 30, 2002; doi:10.1152/ajprenal.00186.2002
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Vol. 283, Issue 6, F1376-F1388, December 2002

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

Marie-Louise Elkjær1, Tae-Hwan Kwon1,2, Weidong Wang1, Jakob Nielsen1, Mark A. Knepper3, Jørgen Frøkiær1, and Søren Nielsen1

1 The Water and Salt Research Center, University of Aarhus, DK-8000 Aarhus C, Denmark; 2 Department of Physiology, School of Medicine, Dongguk University, 780-714 Kyungju, Korea; and 3 Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892

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.

hypokalemia; sodium transport; kidney; urine concentration


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