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Articles in PresS, published online ahead of print August 21, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00272.2002
Submitted on July 25, 2002
Accepted on August 15, 2002
1 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Institute of Experimental Clinical Research, University of Aarhus, Aarhus, Denmark
2 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Department of Cell Biology, University of Aarhus, Denmark
3 Department of Physiology, Dongguk University, Kyungju, Korea, Republic of
4 National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, USA
* To whom correspondence should be addressed. E-mail: jf{at}iekf.au.dk.
We have demonstrated previously that ureteral obstruction was associated with downregulation of renal AQP2 expression and an impaired urinary concentrating capacity. In this study, the changes in expression of major renal sodium transporters were examined in a rat model with 24 hours of unilateral ureteral obstruction (UUO) to clarify the molecular mechanisms of the marked natriuresis seen after release of UUO. Urine collection for 2 hours after release of UUO revealed a significant reduction in urine osmolality, solute-free water reabsorption (TcH2O) 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 ± 14%), type1 bumetanide-sensitive Na-K-2Cl cotransporter (BSC-1; 15 ± 3%) and thiazide-sensitive cotransporter (TSC; 15 ± 4 %). Immunocytochemistry confirmed the downregulation of NHE3, BSC-1, and TSC in response to obstruction. In the non-obstructed contralateral kidney, a significant reduction in the abundance of inner medullary Na,K-ATPase and cortical NaPi-2 were found. This may contribute to the compensatory increase in urine production (7.75 ± 0.91 vs. 3.16 ± 0.26 µl/min/kg), and increased fractional excretion of urinary sodium (1.1 ± 0.2% vs. 0.7 ± 0.1%, P<0.05). In conclusion: 1) 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. 2) Reduced levels of Na,K-ATPase and NaPi-2 in the contralateral non-obstructed kidney may contribute to the compensatory increase of water and sodium excretion from that kidney during UUO and after release of obstruction.
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