Abstract
Cyclooxygenase (COX) constitutes the rate-limiting enzyme in the biosynthetic cascade of prostaglandin (PG). Evidence has accrued suggesting pathophysiological states with altered COX-2 activity and expression. Recent experimental evidence suggests that COX-2 has a pathogenetic role in some of these derangements. In other situations, the effect of altered COX-2 regulation is unclear or possibly beneficial. These processes suggest new areas for potential use of COX-2-specific inhibitors. Conversely, in some conditions COX-2-specific inhibitors should be avoided. The conventional view is that COX-2 is an inducible enzyme. However, COX-2 is also active in the constitutive production of prostanoids in the kidney. Consequently, the pathophysiological states discussed herein include not only COX-2 induction during inflammation but also derangements in COX-2 expression and function caused by non-inflammatory stimuli.
Original language | English (US) |
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Pages (from-to) | S11-S15 |
Journal | Journal of Hypertension |
Volume | 20 |
Issue number | SUPPL. 6 |
DOIs | |
State | Published - Sep 2002 |
Keywords
- Cyclooxygenase-2
- Diabetic nephropathy
- Glomerulonephritis
- Hypertension
- Renal
- Renin
ASJC Scopus subject areas
- Internal Medicine
- Physiology
- Cardiology and Cardiovascular Medicine