Prostaglandin I2 is not major metabolite of arachidonic acid in cultured endothelial cells from human foreskin microvessels

Abstract

Prostaglandin I2 (PGI2), a potent vasodilator and inhibitor of platelet aggregation, is a major product of arachidonic acid metabolism in endothelial cells that are derived from large blood vessels (e.g., umbilical veins). We have examined whether PGI2 is also a major product of arachidonic acid metabolism in cultured endothelial cells that are derived from dermal microvessels in human newborn foreskin. Supernatants from confluent monolayers of endothelial cells that had been incubated for 20 min with [3H]arachidonic acid and the calcium ionophore A23187 (10 μM) were assayed for prostaglandin F(2α) (PGF(2α)), prostaglandin E2 (PGE2), and 6-keto-prostaglandin F(1α) (PGF(1α)) (the stable metabolite of PGI2) by using authentic standards and high performance liquid chromatography. Whereas supernates from stimulated umbilical vein endothelial cells contained 6-keto-PGF(1α) ≥ PGF(2α) ≥ PGE2, supernates from stimulated foreskin microvessel endothelial cells contained PGF(2α) ≃ PGE2 ≥ 6-keto-PGF(1α). Similar results were obtained when supernates from stimulated, unlabeled endothelial cells were analyzed by radioimmunoassay. These data indicate that PGI2 is not a major metabolite of arachidonic acid in cultured endothelial cells from human foreskin microvessels.