Properties of an endogenous arachidonic acid--elicited relaxing mechanism in human placental vessels.

Publication/Presentation Date

10-1-1992

Abstract

OBJECTIVE: Our objective was to examine the action of arachidonic acid on tone in isolated human placental arteries and veins (1 to 2 mm diameter) for mechanisms involving endothelium-derived mediators, the stimulation of guanylate cyclase, and prostaglandin and cytochrome P450 metabolites.

STUDY DESIGN: Pharmacologic probes and endothelium-removal were used to examine the mechanism of relaxation to arachidonic acid (10 nmol/L to 10 mumol/L) observed in placental arteries and veins obtained after delivery from uncomplicated term pregnancies and precontracted with prostaglandin F2 alpha.

RESULTS: Neither removal of the endothelium nor inhibition of prostaglandin biosynthesis with 10 mumol/L indomethacin, arginine-derived nitric oxide formation with 30 mumol/L nitro-L-arginine, or guanylate cyclase stimulation with 10 mumol/L LY83583 altered the observed relaxation to arachidonic acid in either preparation. However, this relaxation was markedly attenuated by 30 mumol/L proadifen (SKF-525A), an inhibitor of cytochrome P450, suggestive of a role for arachidonic acid metabolism by an epoxygenase or monooxygenase pathway.

CONCLUSION: Human placental arteries and veins possess an endogenous mechanism of relaxation to arachidonic acid, which seems to be mediated by metabolites formed by a cytochrome P450 enzyme. This endogenous relaxation mechanism could function as a suppressor of vasospasm in the placental circulation.

Volume

167

Issue

4 Pt 1

First Page

1064

Last Page

1070

ISSN

0002-9378

Disciplines

Medicine and Health Sciences | Pediatrics

PubMedID

1329513

Department(s)

Department of Pediatrics

Document Type

Article

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