Vasorelaxation induced by methyl cinnamate, the major constituent of the essential oil of Ocimum micranthum, in rat isolated aorta

The aim of the present study was to investigate the vascular effects of the E-isomer of methyl cinnamate (E-MC) in rat isolated aortic rings and the putative mechanisms underlying these effects. At 1-3000mol/L, E-MC concentration-dependently relaxed endothelium-intact aortic preparations that had been precontracted with phenylephrine (PHE; 1mol/L), with an IC50 value (geometric mean) of 877.6mol/L (95% confidence interval (CI) 784.1-982.2mol/L). These vasorelaxant effects of E-MC remained unchanged after removal of the vascular endothelium (IC50 725.5mol/L; 95% CI 546.4-963.6mol/L) and pretreatment with 100mol/L N-G-nitro-l-arginine methyl ester (IC50 749.0mol/L; 95% CI 557.8-1005.7mol/L) or 10mol/L 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (IC50 837.2mol/L; 95% CI 511.4-1370.5mol/L). Over the concentration range 1-3000mol/L, E-MC relaxed K+-induced contractions in mesenteric artery preparations (IC50 314.5mol/L; 95% CI 141.9-697.0mol/L) with greater potency than in aortic preparations (IC50 1144.7mol/L; 95% CI 823.2-1591.9mol/L). In the presence of a saturating contractile concentration of K+ (150mmol/L) in Ca2+-containing medium combined with 3mol/L PHE, 1000mol/L E-MC only partially reversed the contractile response. In contrast, under similar conditions, E-MC nearly fully relaxed PHE-induced contractions in aortic rings in a Ba2+-containing medium. In preparations that were maintained under Ca2+-free conditions, 600 and 1000mol/L E-MC significantly reduced the contractions induced by exogenous Ca2+ or Ba2+ in KCl-precontracted preparations, but not in PHE-precontracted preparations (in the presence of 1mol/L verapamil). In addition, E-MC (1-3000mol/L) concentration-dependently relaxed the contractions induced by 2mmol/L sodium orthovanadate. Based on these observations, E-MC-induced endothelium-independent vasorelaxant effects appear to be preferentially mediated by inhibition of plasmalemmal Ca2+ influx through voltage-dependent Ca2+ channels. However, the involvement of a myogenic mechanism in the effects of E-MC is also possible.