Abstract
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 μM to 1 mM showed dose-dependent relaxation of the rat aorta contracted by treatment with prostaglandin F2α, norepinephrine or KCl. In addition, cinnamaldehyde relaxed prostaglandin F2α-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), β-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.
