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1 Institute of Anatomy, Charite - Universitastsmedizin Berlin, Berlin, Germany
2 INSERM U 702, Hopital Tenon, Paris, France
3 Institute of Physiology, Charite - Universitatsmedizin Berlin, Berlin, Germany
4 Zentrum fur Kinder- und Jugendmedizin, Philipps-Universitat Marburg, Marburg, Germany
5 Medizinische Poliklinik, Universitat Munster, Munster, Germany
6 Universite Rene Descartes, Paris, France
7 Institute of Anatomy, Charite - Universitatsmedizin Berlin, Berlin, Germany
* To whom correspondence should be addressed. E-mail: franziska.theilig{at}charite.de.
Renal volume regulation is modulated by the action of cyclooxygenases (COX) and the resulting generation of prostanoids. Epithelial expression of COX isoforms in the cortex directs COX-1 to the distal convolutions and cortical collecting duct, and COX-2 to the thick ascending limb. Partly co-localized are prostaglandin E synthase (PGES), the downstream enzyme for renal prostaglandin E2 (PGE2) generation, and the EP receptors type 1 and 3. COX-1 and related components were studied in 2kidney-1clip (2K1C) Goldblatt hypertensive rats with combined chronic angiotensin (Ang) II- or bradykinin B2-receptor blockade using candesartan (cand) or the B2 antagonist, Hoechst 140 (Hoe). Rats (untreated sham, 2K1C, sham+cand, 2K1C+cand, sham+Hoe, 2K1C+Hoe) were treated to map expression of parameters controlling PGE2 synthesis. In 2K1C, cortical COX isoforms did not change uniformly. COX-2 changed in parallel with NO synthase 1 (NOS1) expression with a raise in the clip, but a decrease in the nonclip side. By contrast, COX-1 and PGES were uniformly downregulated in both kidneys, along with reduced urinary PGE2 levels, and showed no clear relations with the NO status. Ang II receptor blockade confirmed negative regulation of COX-2 by Ang II, but blunted the decrease of COX-1 selectively in nonclip kidneys. B2 receptor blockade reduced COX-2 induction in 2K1C but had no clear effect on COX-1. We suggest that in 2K1C, COX-1 and PGES expression may fail to oppose the effects of renovascular hypertension through reduced prostaglandin signalling in late distal tubule and cortical collecting duct.
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