Release of prostaglandins E2, I2, and D2 from perfused rabbit vascular tissue stimulated by ricinoleic acid

The prelabelling technique (incorporation of (1-¹⁴C)-arachidonic acid was used to investigate the influence of ricinoleic acid on prostaglandin biosynthesis in peripheral vessels. Infusion of ricinoleic acid (0.2 mM) intra-arterially into the isolated perfused ear stimulated the release of labelled arachidonic acid and metabolites. The major metabolite released was PGE₂ followed by PGI₂ (measured as 6-keto-PGF_1α ) and PGD₂ Prostaglandin release was abolished by indometacin (3 μg/ml) and strongly reduced by perfusion with calcium-free, 1 mM EGTA containing solution. In the presence of bovine serum albumin there was a basal release of high amounts of arachidonic acid. Ricinoleic acid tended to increase the released amount of labelled arachidonic acid. In contrast to indometacin, perfusion with calcium-free, 1 mM EGTA containing solution tended to reduce the release of arachidonic acid. The results show that in the peripheral vascular bed ricinoleic acid stimulates the release of arachidonic acid and metabolites probably by activating a calcium-dependent phospholipase A₂. Since ricinoleic acid is well absorbed from the gut, such an effect may occur after ingestion of a highly laxative dose.