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Articles in PresS, published online ahead of print July 30, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00186.2002
Submitted on May 13, 2002
Accepted on July 24, 2002
1 The Water and Salt Research Center, University of Aarhus, 8000 Aarhus C, Denmark
2 The Water and Salt Research Center, University of Aarhus, 8000 Aarhus C, Denmark; Department of Physiology, School of Medicine, Dongguk University, 780-714 Kyungju, Korea, Republic of
3 Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institute of Health, Bethesda, Maryland 20892, USA
* To whom correspondence should be addressed. E-mail: sn{at}ana.au.dk.
The purpose of the study was to examine if hypokalemia is associated with altered abundance of major renal Na+ transporters which may contribute to the development of urinary concentrating defects. We examined the changes in the abundance of NHE3, Na+-K+-ATPase, BSC-1, TSC and ENaC subunits in kidneys of hypokalemic rats. Semiquantitative immunoblotting revealed that the abundance of the bumetanide-sensitive Na+-K+-2Cl- cotransporter BSC-1 (57%) and the thiazide-sensitive NaCl cotransporter TSC (46%) were profoundly decreased in ISOM and Cortex/OSOM, respectively. These findings were confirmed by immunohistochemistry. Moreover, total kidney abundance of all ENaC subunits were significantly reduced in response to hypokalemia: 
-subunit (61%), ß-subunit (41%), and 
-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 sodium loss and/or to maintain the intracellular pH levels.
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