Clinical and experimental pharmacology & physiology

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

PMID 25115734


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 1-3000xa0μmol/L, E-MC concentration-dependently relaxed endothelium-intact aortic preparations that had been precontracted with phenylephrine (PHE; 1xa0μmol/L), with an IC50 value (geometric mean) of 877.6xa0μmol/L (95% confidence interval (CI) 784.1-982.2xa0μmol/L). These vasorelaxant effects of E-MC remained unchanged after removal of the vascular endothelium (IC50 725.5xa0μmol/L; 95% CI 546.4-963.6xa0μmol/L) and pretreatment with 100xa0μmol/L N(G) -nitro-l-arginine methyl ester (IC50 749.0xa0μmol/L; 95% CI 557.8-1005.7xa0μmol/L) or 10xa0μmol/L 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (IC50 837.2xa0μmol/L; 95% CI 511.4-1370.5xa0μmol/L). Over the concentration range 1-3000xa0μmol/L, E-MC relaxed K(+) -induced contractions in mesenteric artery preparations (IC50 314.5xa0μmol/L; 95% CI 141.9-697.0xa0μmol/L) with greater potency than in aortic preparations (IC50 1144.7xa0μmol/L; 95% CI 823.2-1591.9xa0μmol/L). In the presence of a saturating contractile concentration of K(+) (150xa0mmol/L) in Ca(2+) -containing medium combined with 3xa0μmol/L PHE, 1000xa0μmol/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 Ba(2+) -containing medium. In preparations that were maintained under Ca(2+) -free conditions, 600 and 1000xa0μmol/L E-MC significantly reduced the contractions induced by exogenous Ca(2+) or Ba(2+) in KCl-precontracted preparations, but not in PHE-precontracted preparations (in the presence of 1xa0μmol/L verapamil). In addition, E-MC (1-3000xa0μmol/L) concentration-dependently relaxed the contractions induced by 2xa0mmol/L sodium orthovanadate. Based on these observations, E-MC-induced endothelium-independent vasorelaxant effects appear to be preferentially mediated by inhibition of plasmalemmal Ca(2+) influx through voltage-dependent Ca(2+) channels. However, the involvement of a myogenic mechanism in the effects of E-MC is also possible.