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1 The Water and Salt Research Center and 3 Department of Cell Biology, Institute of Anatomy, University of Aarhus, DK-8000 Aarhus C; 2 Institute of Experimental Clinical Research and 6 Department of Clinical Physiology, Aarhus University Hospital-Skejby, University of Aarhus, DK-8200 Aarhus N, Denmark; 4 Department of Physiology, School of Medicine, Dongguk University, Kyungju 780-714, Korea; and 5 Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892
It has been demonstrated previously
that ureteral obstruction was associated with downregulation of renal
AQP2 expression and an impaired urinary concentrating capacity (Li C,
Wang W, Kwon TH, Isikay L, Wen JG, Marples D, Djurhuus JC, Stockwell A, Knepper MA, Nielsen S, and Frøkiær J. Am J Physiol Renal
Physiol 281: F163-F171, 2001). In the present study, changes
in the expression of major renal Na transporters were examined in a rat
model with 24 h of unilateral ureteral obstruction (UUO) to
clarify the molecular mechanisms of the marked natriuresis seen after
release of UUO. Urine collection for 2 h after release of UUO
revealed a significant reduction in urinary osmolality, solute-free
water reabsorption, and a marked natriuresis (0.29 ± 0.03 vs.
0.17 ± 0.03 µmol/min, P < 0.05). Consistent with
this, immunoblotting revealed significant reductions in the abundance
of major renal Na transporters: type 3 Na+/H+
exchanger (NHE3; 24 ± 4% of sham-operated control levels), type 2 Na-Pi cotransporter (NaPi-2; 21 ± 4%), Na-K-ATPase
(37 ± 4%), type 1 bumetanide-sensitive Na-K-2Cl cotransporter
(BSC-1; 15 ± 3%), and thiazide-sensitive Na-Cl cotransporter
(TSC; 15 ± 4%). Immunocytochemistry confirmed the downregulation
of NHE3, BSC-1, and TSC in response to obstruction. In nonobstructed
contralateral kidneys, a significant reduction in the abundance of
inner medullary Na-K-ATPase and cortical NaPi-2 was found. This may
contribute to the compensatory increase in urinary production (23 ± 2 vs. 13 ± 1 µl · min
1 · kg1)
and increased fractional excretion of urinary Na (0.62 ± 0.03 vs.
0.44 ± 0.03%, P < 0.05). In conclusion,
downregulation of major renal Na transporters in rats with UUO may
contribute to the impairment in urinary concentrating capacity and
natriuresis after release of obstruction, and reduced levels of
Na-K-ATPase and NaPi-2 in the contralateral nonobstructed kidney may
contribute to the compensatory increase in water and Na excretion from
that kidney during UUO and after release of obstruction.
thick ascending limb of Henle's loop; collecting duct; proximal tubule; distal convoluted tubule; obstructive nephropathy; sodium excretion
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