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Articles in PresS, published online ahead of print April 2, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00326.2001
Submitted on October 26, 2001
Accepted on March 30, 2002
1 Department of Medicine, Renal Division, Emory University, Atlanta, GA, USA
2 Department of Pathology, Emory University, Atlanta, GA, USA
3 Department of Medicine, Renal Division, Emory University, Atlanta, GA, USA; Department of Physiology, Emory University, Atlanta, GA, USA
* To whom correspondence should be addressed. E-mail: ajprenal{at}emory.edu.
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 a normal medullary histology and creatinine clearance. To explore the urine concentrating defect in ACE.2 mice, renal medullary transport proteins were analyzed using western analysis. In the inner medulla, UT-A1, ClC-K1, and AQP1 were significantly reduced to 28±5%, 6±6%, and 39±5% of the level in wild-type mice, respectively, while AQP2 and UT-B were unchanged. In outer medulla, NKCC2/BSC1 and AQP1 were significantly reduced to 56±11% and 29±6%, respectively, while Na+/K+-ATPase, UT-A2, UT-B, and AQP2 were unchanged, and ROMK 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 back-crossed onto a Black 6 or a Swiss background and was not rescued by angiotensin II infusion. We conclude that the urine concentrating defect in ACE.2 mice is associated with, and may result from, down-regulation of some or all of these key urea, salt, and water transport proteins.
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