Pathophysiology of cyclooxygenases in cardiovascular homeostasis

Rani S. Sellers, Z. A. Radi, N. K. Khan

Research output: Contribution to journalArticle

24 Scopus citations

Abstract

Cyclooxygenase (COX) catalyzes the conversion of arachidonic acid into prostaglandin H2 (PGH2), which is subsequently converted to the prostanoids PGE2, PGI2, PGF, and thromboxane A2. COX has 2 distinct membrane-anchored isoenzymes: COX-1 and COX-2. COX-1 is constitutively expressed in most normal tissues; COX-2 is highly induced by proinflammatory mediators in the setting of inflammation, injury, and pain. Inhibitors of COX activity include conventional nonselective nonsteroidal anti-inflammatory drugs and selective nonsteroidal anti-inflammatory drugs, such as COX-2 inhibitors. The adverse effects of COX inhibitors on the cardiovascular system have been addressed in the last few years. In general, COX inhibitors have many effects, but those most important to the cardiovascular system can be direct (through the effects of prostanoids) and indirect (through alterations in fluid dynamics). Despite reports of detrimental human cardiovascular events associated with COX inhibitors, short, long, and lifetime preclinical toxicology studies in rodents and nonrodents have failed to identify these risks. This article focuses on the expression and function of COX enzymes in normal and pathologic conditions of the cardiovascular system and discusses the cardiovascular pathophysiologic complications associated with COX inhibition.

Original languageEnglish (US)
Pages (from-to)601-613
Number of pages13
JournalVeterinary Pathology
Volume47
Issue number4
DOIs
StatePublished - Jul 30 2010

Keywords

  • COX-1
  • COX-2
  • Cardiovascular
  • Cyclooxygenase
  • NSAIDs
  • Nonselective nonsteroidal anti-inflammatory drugs
  • Selective nonsteroidal anti-inflammatory drugs

ASJC Scopus subject areas

  • veterinary(all)

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