Eicosapentaenoic acid (EPA)-induced inhibitory effects on porcine coronary and cerebral arteries involve inhibition of prostanoid TP receptors

This study was performed to elucidate whether eicosapentaenoic acid (EPA) suppresses spasm-prone blood vessel contractions induced by a thromboxane mimetic (U46619) and prostaglandin F-2 alpha (PGF(2 alpha)) and determine whether the primary target of EPA is the prostanoid TP receptor. Accordingly, we assessed: (1) the tension changes in porcine basilar and coronary arteries, and (2) changes in the Fura-2 (an intracellular Ca2+ indicator) fluorescence intensity ratio at 510 nm elicited by 340/380 nm excitation (F340/380) in 293T cells expressing the human TP receptor (TP-293T cells) and those expressing the human prostanoid FP receptor (FP-293T cells). EPA inhibited both porcine basilar and coronary artery contractions induced by U46619 and PGF(2 alpha) in a concentration-dependent manner, but it did not affect the contractions induced by 80 mM KCl. EPA also inhibited the increase in F340/380 induced by U46619 and PGF(2 alpha) in TP-293T cells. In contrast, EPA showed only a marginal effect on the increase in F340/380 induced by PGF(2 alpha) in FP-293T cells. These findings indicate that EPA strongly suppresses the porcine basilar and coronary artery contractions mediated by TP receptor and that inhibition of TP receptors partly underlies the EPA-induced inhibitory effects on these arterial contractions.

Automated summary

This study demonstrates that EPA can effectively suppress spasm-prone blood vessel contractions mediated by TP receptors, indicating its potential therapeutic value in preventing arterial spasms.