Possible contribution of platelet cyclooxygenase to the renal vascular action of 5,6-epoxyeicosatrienoic acid

David Fulton, Michael Balazy, John C. McGiff, John Quilley

Research output: Contribution to journalArticle

24 Scopus citations

Abstract

5,6-Epoxyeicosatrienoic acid (5,6-EET), a cytochrome P450-dependent arachidonate product, is a substrate for cyclooxygenase (COX) and, in some vascular preparations, elicits COX-dependent vasodilation. In the blood perfused rat kidney, 5,6-EET causes COX-dependent renal vasoconstriction, whereas in the rat isolated kidney perfused with a physiological buffer, 5,6- EET produces dose-dependent vasodilation that is unaffected by indomethacin. We examined the possible contribution of platelet COX to the vasoconstrictor action of 5,6-EET. Incubation of labeled 5,6-EET with rat washed platelets yields additional products that elute between 14 to 17 rain on high- performance liquid chromatography (HPLC) and cause constriction of the perfused kidney. Indomethacin decreased the formation of these products and reduced the vasoconstrictor capacity of the corresponding HPLC fractions. Thus, platelet COX can metabolize 5,6-EET to vasoconstrictor products that may contribute to the in vivo vasoconstrictor effect of this eicosanoid.

Original languageEnglish (US)
Pages (from-to)1195-1199
Number of pages5
JournalJournal of Pharmacology and Experimental Therapeutics
Volume277
Issue number3
StatePublished - Jun 1 1996
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology

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