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标题：Vasodilatory effects of cinnamaldehyde and its mechanism of action in the rat aorta
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作者：Yong-Liang Xue ; Hai-Xia Shi ; Ferid Murad 等
期刊名称：Vascular Health and Risk Management
印刷版ISSN：1176-6344
电子版ISSN：1178-2048
出版年度：2011
卷号：7
页码：273-280
DOI：10.2147/VHRM.S15429
出版社：Dove Medical Press Ltd
摘要：The vasodilatory effect of cinnamaldehyde was investigated for its mechanism of action using isolated rings of rat aorta. Cinnamaldehyde relaxed aortic rings precontracted with phenylephrine in a dose-dependent manner, was not affected by either the presence or removal of the endothelium. Pretreatment with NG-nitro-L-arginine methyl ester and 1H-[1,2,4]-oxadiazole-[4,3-a]-quinoxalin-1-one could not block vasodilation by cinnamaldehyde, indicating that nitric oxide signaling is not involved. Potassium channel blockers, such as glibenclamide, tetraethylammonium, and BaCl₂, had no effect on the relaxation produced by cinnamaldehyde. In addition, treatment with either indomethacin or propranolol did not affect cinnamaldehyde-induced vasodilatation. On the other hand, pretreatment of endothelium-denuded rings with cinnamaldehyde significantly inhibited vasoconstriction induced by endogenous vasoconstrictors, including angiotensin II, 5-hydroxytryptamine, dopamine, endothelin-1, and phenylephrine. In a Ca²⁺-free experimental setting, this natural vasodilator not only blocked Ca²⁺ influx-dependent vasoconstriction by either phenylephrine or KCl, but also inhibited phenylephrine-induced tonic contraction, which relies on intracellular Ca²⁺ release. This study shows that endothelium-independent, Ca²⁺ influx and/or an inhibitory release mechanism contributes to the vasodilatory effect of cinnamaldehyde.
关键词：cinnamaldehyde; vasodilation; endothelium; vascular smooth muscle cell