Abstract
OBJECTIVE: Our objective was to examine the action of arachidonic acid on tone in isolated humanplacental 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 mechanismof relaxation to arachidonic acid (10 nmol/L to 10 μmol/L) observed in placental arteries and veins obtained after delivery from uncomplicated term pregnancies and precontracted with prostaglandin F 2a. RESULTS: Neither removal of the endothelium nor inhibition of prostaglandin biosynthesis with 10 μmol/Lindomethacin, arginine-derived nitric oxide formation with 30 μmol/L nitro- l-arginine, or guanylate cyclase stimulation with 10 μmol/L LY83583 altered the observed relaxation to arachidonic acid in either preparation. However, this relaxation was markedly attenuated by 30 μmol/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 toarachidonic 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. ( Am J Obstet Gynecol 1992;167:1064–70.)
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