Mechanisms underlying the endothelium-dependent vasodilatory effect of an aqueous extract of Elaeis guineensis Jacq. (Arecaceae) in porcine coronary artery rings

This study was undertaken to investigate the vasodilatory effect of an aqueous extract of Elaeis guineensis Jacq (EGE) in the porcine coronary artery and, if so, to characterize the underlying mechanism. In the presence of indomethacin to prevent the formation of prostanoids, EGE caused pronounced relaxations in coronary artery rings with endothelium but not in those after mechanical removal of endothelial cells. Relaxations to EGE were significantly reduced by Nï·-nitro-L-arginine (L-NA, a competitive inhibitor of NO synthase), slightly but not significantly by charybdotoxin plus apamin (two potent inhibitors of EDHF-mediated responses) and abolished by the combination of L-NA and charybdotoxin plus apamin. Relaxations to EGE were abolished by the membrane permeant SOD mimetic, MnTMPyP, and significantly reduced by wortmannin, an inhibitor of PI3-kinase. Exposure of endothelial cells to EGE increased the phosphorylation level of eNOS at Ser1177 in a time and concentration-dependent manner. MnTMPyP abolished the EGE-induced phosphorylation of eNOS. In conclusion, these data indicate that EGE induces pronounced endothelium-dependent relaxations of the porcine coronary artery, which involve predominantly NO. The stimulatory effect of EGE on eNOS involves the redox-sensitive phosphorylation of eNOS at Ser1177 most likely via the PI3-kinase pathway.