Renal COX-2, Cytokines and 20-HETE: Tubular and Vascular Mechanisms

Author(s): Nicholas R. Ferreri, John C. McGiff, Mairead A. Carroll, John Quilley

Journal Name: Current Pharmaceutical Design

Volume 10 , Issue 6 , 2004

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Our initial studies on renal cyclooxygenase (COX)-2 expression and activity addressed the critical role of angiotensin II (Ang II) in increasing tumor necrosis factor alpha (TNF) that eventuated in expression of COX-2 in the medullary thick ascending limb (mTAL) of the nephron. COX-2 supplanted the dominant oxygenase, the cytochrome P450 (CYP) enzyme, w- hydroxylase, that synthesized 20-hydroxyeicosatetraenoic acid (20-HETE). These findings served as the basis for additional studies on: 1) the role of glucocorticoids in regulating COX-2 expression and activity in the mTAL; and 2) the utilization of the same signaling pathways in response to stimulation of the mTAL calcium receptor (CaR). These studies of mTAL COX-2 expression which are addressed in the first part of this chapter are followed by explorations of the expression of COX-2 in preglomerular microvessels (PGMV) and the relationship of COX-2 to 20- HETE, the principal eicosanoid of PGMV. The third and last component of this chapter explores the signaling events, focusing on COX-2, which are set in motion by diabetes.

Keywords: calcium receptor (car), cyclooxygenase (cox)-2, diabetes, hypertension, prostaglandin e2 (pge2), thick ascending limb (tal), tumor necrosis factor alpha (tnf), 20-hydroxyeicosatetraenoic acid (20-hete)

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Article Details

Year: 2004
Page: [613 - 626]
Pages: 14
DOI: 10.2174/1381612043453063
Price: $65

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