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Renal cortical regulation of COX-1 and functionally related products in early renovascular hypertension (rat)

Departments of ¹Anatomy and ²Physiology, Charité Berlin, Berlin; ³Institut National de la Santé et de la Recherche Médicale U 702, Hôpital Tenon, Paris; ⁴Zentrum für Kinder u. Jugendmedizin, Marburg, Germany; ⁵Medizinische Poliklinik, Münster, Germany; and ⁶Institut National de la Santé et de la Recherche Médicale U 652, Université René Descartes, Paris, France

Submitted 27 March 2006 ; accepted in final form 7 June 2006

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 colocalized 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 two kidney-one clip (2K1C) Goldblatt hypertensive rats with combined chronic 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 clipped, but a decrease in the nonclipped 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 in COX-1 selectively in nonclipped 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 signaling in late distal tubule and cortical collecting duct.

cyclooxygenase; nitric oxide synthase; bradykinin

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