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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:
-subunit (61%), 
-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
Na+ loss and/or to maintain intracellular pH levels.
hypokalemia; sodium transport; kidney; urine concentration
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