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Vasodilatory effects of cinnamaldehyde and its mechanism of action in the rat aorta

Authors Xue Y, Hai-xia Shi, Murad F, Bian K

Published 28 April 2011 Volume 2011:7 Pages 273—280


Review by Single anonymous peer review

Peer reviewer comments 4

Yong-Liang Xue1, Hai-Xia Shi1, Ferid Murad1,2, Ka Bian1,2
1Murad Research Institute for Modernized Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, People’s Republic of China; 2E-Institute of Shanghai Universities, Division of Nitric Oxide and Inflammatory Medicine, Shanghai, People’s Republic of China

Abstract: 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.

Keywords: cinnamaldehyde, vasodilation, endothelium, vascular smooth muscle cell

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