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1 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Department of Endocrinology, Diabetes and Metabolism, University Children's Hospital, Ljubljana, Slovenia
2 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Institute of Anatomy, University of Aarhus, Aarhus, Denmark
3 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Department of Biochemistry and Cell Biology, Kyungpook National University, Taegu, Korea, Republic of
4 Department of Endocrinology, Diabetes and Metabolism, University Children's Hospital, Ljubljana, Slovenia
5 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Institute of Experimental Clinical Research, University of Aarhus, Aarhus, Denmark
* To whom correspondence should be addressed. E-mail: sn{at}ana.au.dk.
Prostaglandins have an important role in renal salt and water re-absorption. PGE2 is the main kidney prostaglandin and is thought to be mainly produced in the kidney inner medulla (IM). There are indications that PGE2 synthesis in nephrogenic (NDI) and central (CDI) diabetes insipidus is altered. We hypothesize that the expression of the major PGE2 synthesis enzymes; cyclooxygenases 1 and 2 (COX-1, COX-2) and membrane-associated prostaglandin E2 synthase (mPGES) is altered in the kidneys of the rats with NDI and CDI. Wistar rats treated with lithium for four weeks were used as NDI model. Half of the NDI model rats were additionally dehydrated for 48 hours. Brattleboro (BB) rats that lack endogenous antidiuretic hormone were used as CDI model. Expression and localization of COX-1, COX-2 and mPGES in IM, inner stripe of outer medulla (ISOM) and cortex were determined by immunobloting and immunohistochemistry. In lithium-induced NDI expression of COX-1, COX-2 and mPGES was markedly decreased in IM. In ISOM and cortex COX-1 expression was marginally reduced and mPGES expression was unaltered. COX-2 expression was undetected in ISOM and marginally increased in cortex. Consistent with this the density of COX-2 expressing cells in macula densa was significantly increased, indicating differential regulation of COX-2 in IM and cortex. Dehydration of NDI rats resulted in a marked increase of COX-2 immunolabeling in IM interstitial cells and there was no significant change in COX-1 and mPGES expression in any kidney zone. Treatment of dDAVP in BB rats for 6 days resulted in a markedly increased expression of COX-1, COX-2 and mPGES in IM. In cortex there were no changes in the expression of COX-1 and mPGES, whereas COX-2 expression was decreased. These results identify markedly reduced expression of COX-1, COX-2 and mPGES in IM in lithium-induced NDI. Furthermore there were major changes in the expression of COX-1, COX-2 and mPGES in rats with CDI.
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