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Am J Physiol Renal Physiol 283: F517-F524, 2002. First published April 2, 2002; doi:10.1152/ajprenal.00326.2001
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Vol. 283, Issue 3, F517-F524, September 2002

Impaired urine concentration and absence of tissue ACE: involvement of medullary transport proteins

Janet D. Klein1,*, D. Le Quach2,*, Justin M. Cole2, Kevin Disher2, Anne K. Mongiu2, Xiaodan Wang1, Kenneth E. Bernstein2, and Jeff M. Sands1,3

1 Renal Division, Department of Medicine, 2 Department of Pathology, and 3 Department of Physiology, Emory University School of Medicine, Atlanta, Georgia 30322

ACE.2 mice lack all tissue angiotensin-converting enzyme (ACE) but have 33% of normal plasma ACE activity. They exhibit the urine-concentrating defect and hyperkalemia present in mice that lack all ACE, but in contrast to the complete knockout, ACE.2 mice have normal medullary histology and creatinine clearance. To explore the urine-concentrating defect in ACE.2 mice, renal medullary transport proteins were analyzed using Western blot analysis. In the inner medulla, UT-A1, ClC-K1, and aquaporin-1 (AQP1) were significantly reduced to 28 ± 5, 6 ± 6, and 39 ± 5% of the level in wild-type mice, respectively, whereas AQP2 and UT-B were unchanged. In the outer medulla, Na+-K+-2Cl- cotransporter (NKCC2/BSC1) and AQP1 were significantly reduced to 56 ± 11 and 29 ± 6%, respectively, whereas Na+-K+-ATPase, UT-A2, UT-B, and AQP2 were unchanged, and renal outer medullary potassium channel was significantly increased to 711 ± 187% of the level in wild-type mice. The abnormal expression of these transporters was similar in ACE.2 mice backcrossed onto a C57BL/6 or a Swiss background and was not rescued by ANG II infusion. We conclude that the urine-concentrating defect in ACE.2 mice is associated with, and may result from, downregulation of some or all of these key urea, salt, and water transport proteins.

urine-concentrating mechanism; angiotensin; urea; sodium chloride; potassium; aquaporin; angiotensin-converting enzyme

* J. D. Klein and D. Le Quach contributed equally to this work.




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