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

Summary 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 1–3000  μ mol/L, E‐ MC concentration‐dependently relaxed endothelium‐intact aortic preparations that had been precontracted with phenylephrine ( PHE ; 1  μ mol/L), with an IC 50 value (geometric mean) of 877.6  μ mol/L (95% confidence interval ( CI ) 784.1–982.2  μ mol/L). These vasorelaxant effects of E‐ MC remained unchanged after removal of the vascular endothelium ( IC 50 725.5  μ mol/L; 95% CI 546.4–963.6  μ mol/L) and pretreatment with 100  μ mol/L N G ‐nitro‐ l ‐arginine methyl ester ( IC 50 749.0  μ mol/L; 95% CI 557.8–1005.7  μ mol/L) or 10  μ mol/L 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one ( IC 50 837.2  μ mol/L; 95% CI 511.4–1370.5  μ mol/L). Over the concentration range 1–3000  μ mol/L, E‐ MC relaxed K + ‐induced contractions in mesenteric artery preparations ( IC 50 314.5  μ mol/L; 95% CI 141.9–697.0  μ mol/L) with greater potency than in aortic preparations ( IC 50 1144.7  μ mol/L; 95% CI 823.2–1591.9  μ mol/L). In the presence of a saturating contractile concentration of K + (150 mmol/L) in Ca 2+ ‐containing medium combined with 3  μ mol/L PHE , 1000  μ mol/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 1000  μ mol/L E‐ MC significantly reduced the contractions induced by exogenous Ca 2+ or Ba 2+ in KC l‐precontracted preparations, but not in PHE ‐precontracted preparations (in the presence of 1  μ mol/L verapamil). In addition, E‐ MC (1–3000  μ mol/L) concentration‐dependently relaxed the contractions induced by 2 mmol/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.