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

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.

Cardiovascular Activity of the Chemical Constituents of Essential Oils

“…When carried in micelles, cinnamaldehyde was also able to induce endothelium-dependent vascular relaxation by NO- and H 2 O 2 -dependent means. This was also demonstrated by Xue et al [ 43 ], who showed that this relaxant effect of cinnamaldehyde was likely mediated by changes in calcium influx or in its release from intracellular stores. Additionally, Alvarez-Collazo et al [ 44 ] studied the mechanism of action of this compound and showed that CA promoted relaxation in vascular smooth muscle cells (VSMC) and ventricular cardiac myocytes (VCM), at least in part by inhibition of the L-Type Ca 2+ channel.…”

Investigating the potential role of TRPA1 in locomotion and cardiovascular control during hypertension

“…Cinnamaldehyde (CA) is a commonly used TRPA1 agonist, selected due to its relative selectivity and potency (Bandell et al 2004 ). It has been shown to cause vasorelaxation and vasodilation in several studies (VanderEnde and Morrow 2001 ; Namer et al 2005 ; Yanaga et al 2006 ; Pozsgai et al 2010 ; Xue et al 2011 ). Our group has also recently demonstrated CA induced ex vivo vasorelaxation and in vivo vasodilation responses to be significantly reduced in TRPA1 knockout (KO) mice (Pozsgai et al 2010 ).…”

“…In line with the role for TRPA1 in inflammation, several groups demonstrate TRPA1 agonists to cause vasorelaxation or vasodilation, occurring in a range of species and vascular beds (Bodkin and Brain 2010 ). TRPA1-induced vasorelaxation is commonly identified to be neuropeptide mediated (Louis et al 1989 ; Morris et al 1999 ; Hikiji et al 2000 ; Grant et al 2005 ; Namer et al 2005 ; Graepel et al 2011 ; Kunkler et al 2011 ), while other studies propose direct changes in calcium handling (Yanaga et al 2006 ; Earley et al 2009 ; Xue et al 2011 ).…”

Ameliorative impact of cinnamon against high blood pressure; an updated review

“…In 2011, Xue et al indicated that cinnamaldehyde increased rat vascular smooth muscle in an endotheliumindependent method. The capability of cinnamaldehyde in vasodilatory performance might be due to inhibition of both Ca 2+ invasion and Ca 2+ discharge (39). Likewise, cinnamaldehyde prevents the development of hypertension in types I and II diabetes by reducing vascular contractility, as well as its insulinotropic effect in insulin fault (40).…”