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Study on the Mechanism of Vascular Relaxation Induced by Cortex Caryphylli  

Song, Chul-Min (College of Oriental Medicine, Wonkwang University)
Shin, Sun-Ho (College of Oriental Medicine, Wonkwang University)
Jung, Hyun-Ae (College of Oriental Medicine, Wonkwang University)
Lee, Jun-Kyoung (Professional Graduate School of Orienal Medicine, Wonkwang University)
Cao, Li-Hua (Professional Graduate School of Orienal Medicine, Wonkwang University)
Kang, Dae-Gil (Professional Graduate School of Orienal Medicine, Wonkwang University)
Lee, Ho-Sup (Professional Graduate School of Orienal Medicine, Wonkwang University)
Publication Information
Journal of Physiology & Pathology in Korean Medicine / v.20, no.5, 2006 , pp. 1166-1173 More about this Journal
Abstract
The aqueous extracts of Cortex Caryophylli (AEC) induced dose-dependent relaxation of phenylephrine-precontracted aorta, which was abolished by removal of functional endothelium. Pretreatment of the endothelium-intact aortic tissues with N$^G$_nitro-L-arginine methyl ester (L-NAME) or 1 H-[1,2,4]-oxadiazole-[4,3-${\alpha}$l-quinoxalin-1-one (ODQ) inhibited the relaxation induced by AEC. AEC-induced vascular relaxations were also markedly attenuated by addition of verapamil, diltiazem and glibenclamide, tetraethylammonium (TEA), respectively, while the relaxation effect of AEC was not blocked by indomethacin, atropine, or propranolol. Moreover, incubation of endothelium-intact aortic rings with AEC increased the production of cGMP. These results suggest that AEC dilates vascular smooth muscle via endothelium-dependent nitric oxide/cGMP signaling, which seems to be causally related with L-type Ca$^{2+}$ and K$^+$ channels.
Keywords
aqueous extracts of Cortex Caryophylli (AEC); NO/cGMP; vasodilation;
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