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Articles in PresS, published online ahead of print November 13, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.00250.2001
Submitted on August 10, 2001
Accepted on November 5, 2001
1 Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood, Bethesda, MD, USA
2 Water and Salt Research Center, Univ. of Aarhus, Aarhus, DK, Denmark
* To whom correspondence should be addressed. E-mail: knep{at}helix.nih.gov.
Clinical disorders of extracellular fluid (ECF) volume regulation are often associated with changes in plasma urea concentration. To investigate possible renal causes, we measured the relative abundances of the urea transporters UTA-1, UTA-2 and UTA-3 in renal medulla of rats with aldosterone-induced NaCl retention. ECF volume-expanded rats received aldosterone by osmotic minipump plus a diet containing a high level of NaCl. Control rats received the same infusion of aldosterone plus a virtually NaCl free diet, which prevented the ECF volume expansion. Preliminary measurements demonstrated transient positive Na and water balance, decreased serum urea concentration and increased urea clearance, but no change in creatinine clearance. Immunoblotting of homogenates from inner medulla showed a marked decrease in the abundances of the collecting duct urea transporters, UTA-1 and UTA-3. There were no differences in abundances of UTA-2, aquaporin-2, aquaporin-3, or aquaporin-4 in ECF volume-expanded rats versus controls. Time-course experiments demonstrated that changes in UTA-1 abundance paralleled the fall in serum urea concentration after switching from a low- to a high-NaCl diet, while the fall in UTA-3 abundance was delayed. Candesartan administration markedly decreased the abundances of UTA-1 and UTA-3 in renal inner medulla, consistent with a role for the AT1 angiotensin II receptor in urea transport regulation. The results support the view that ECF-related changes in serum urea concentration are mediated at least in part through altered urea transporter abundances.
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