Cinnamaldehyde induces endothelium-dependent and -independent vasorelaxant action on isolated rat aorta.

The vasorelaxant effect of cinnamaldehyde, one of the major oil components in Cinnamomi Cortex, was studied using isolated rat aorta. Cinnamaldehyde at final concentrations of 1 microM to 1 mM showed dose-dependent relaxation of the rat aorta contracted by treatment with prostaglandin F2alpha, norepinephrine or KCl. In addition, cinnamaldehyde relaxed prostaglandin F2alpha-precontracted aortic rings with endothelium and without endothelium, with the latter being significantly less sensitive than the former. Relaxation induced by cinnamaldehyde with endothelium was significantly inhibited by NG-nitro-L-arginine methyl ester (L-NAME), while nonselective cyclooxygenase inhibitor (indomethacin), beta-adrenergic receptor blocker (propranolol), an inhibitor of phosphodiesterase (theophylline), a delayed rectifier K+ channel blocker (tetraethyl ammonium chloride), or an ATP-sensitive K+ channel blocker (glibenclamide) did not reduce the relaxation induced by cinnamaldehyde with endothelium treated by L-NAME. Conversely, aorta pretreatment with L-NAME and theophylline increased the relaxation by cinnamaldehyde significantly compared to aorta pretreatment with only L-NAME. Furthermore, cinnamaldehyde significantly inhibited Ca2+-induced contraction. These results suggested that the vasorelaxant effects of cinnamaldehyde were derived from both endothelium-dependent and -independent effects. Endothelium-dependent relaxation is affected by nitric oxide, and one of the mechanisms of endothelium-independent relaxation is thought to be influenced by the blocking of Ca2+ channels.