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1 Department of Internal Medicine, University of Utah, Salt Lake City, UT, USA; Veterans Affairs Medical Center, Salt Lake City, UT, USA
2 Department of Genetics, University of Utah, Salt Lake City, UT, USA
3 Department of Internal Medicine, University of Utah, Salt Lake City, UT, USA
4 Department of Pediatrics, University of Utah, Salt Lake City, UT, USA
* To whom correspondence should be addressed. E-mail: tianxin.yang{at}hsc.utah.edu.
Expression of COX-2, but not COX-1, in the renal medulla is stimulated by chronic salt loading yet the functional implication of this phenomenon is incompletely understood. The present study examined the cellular localization and anti-hypertensive function of high salt-induced COX-2 expression in the renal medulla with a parallel assessment of the function of COX-1. The induced COX-2 protein expression in response to high salt loading, assessed by immunostaining, was found predominantly in inner medullary interstitial cells, while COX-1 protein was abundant in both collecting duct (CD) and inner medullary interstitial cells, and was not affected by high salt. We compared mRNA expressions of COX-1 and -2 in CD versus non-collecting duct cells (non-CD) isolated from AQP2-GFP transgenic mice. A low level of COX-2 mRNA but a high level of COX-1 mRNA, as determined by real time RT-PCR, were detected in the CD as compared to non-CD segments. During high salt intake, chronic infusions of the COX-2 blocker, NS-398, and the COX-1 blocker, SC-560, into the renal medulla of Sprague-Dawley rats for 5 days induced increases in MAP by approximately 30 and 15 mmHg, respectively. During similar high salt intake, COX-1 KO mice exhibited a gradual but significant increase in systolic blood pressure that was associated with a marked suppression of urinary PGE2 excretion. Therefore, we conclude that the two COX isoforms in the renal medulla play a similar role in the stabilization of arterial blood pressure during salt loading.
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