title: Endothelium-dependent and direct relaxation induced by ethyl acetate extract from Flos Chrysanthemi in rat thoracic aorta.
abstract: The aims of the present study were to investigate the vasoactive effects of ethyl acetate extract from Flos Chrysanthemi (FCE) and its mechanisms on the rat thoracic aorta. FCE (9.4-150 mg/L) caused a concentration-dependent relaxation on endothelium-intact rings precontracted with phenylephrine (PE, 10(-6)M) or a high level of K+ (6x10(-2)M). By removal of endothelium, the effect was not abolished but reduced significantly. N(G)-nitro-l-arginine methyl ester (l-NAME) (10(-4) M), methylene blue (10(-5) M) significantly inhibited the effect of FCE. Meanwhile, NO synthase of aorta in FCE group was markedly elevated versus the control. However, indomethacin did not influence FCE effect. SKF-525A combined with l-NAME had the same effect as l-NAME. Tetraethylammonium, BaCl2, 4-aminopyridine, 5-HD and propranolol also did not influence the vascular effect of FCE, but glibenclamide significantly attenuated its vasodilation. FCE did not reduce PE-induced transient contraction in Ca(2+)-free medium, but inhibited PE-induced contraction in K(+)-free solution or Ca2+ caused contraction after PE induced a stable contraction in Ca(2+)-free solution. It is concluded that FCE induced both endothelium-dependent and -independent relaxation. NO and cGMP-mediated pathway are likely involved in the endothelium-dependent relaxation, whereas inhibition of voltage-dependent Ca2+ channel, receptor-operate Ca2+ channel and activation of K(ATP) contribute in part to the endothelium-independent relaxation.
authors.affiliation: College of Pharmaceutical Sciences, Zhejiang University, 353 Yan'an Road, Hangzhou 310031, China. hdjiang@zju.edu.cn
authors.forename: Hui-Di
authors.initials: HD
authors.lastname: Jiang
authors.forename: Jun
authors.initials: J
authors.lastname: Cai
authors.forename: Juan-Hua
authors.initials: JH
authors.lastname: Xu
authors.forename: Xin-Mei
authors.initials: XM
authors.lastname: Zhou
authors.forename: Qiang
authors.initials: Q
authors.lastname: Xia
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects* / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology; D031202:Chrysanthemum / Q000737:chemistry*; D004730:Endothelium, Vascular / Q000502:physiology*; D035264:Flowers / Q000737:chemistry*; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D008751:Methylene Blue / Q000494:pharmacology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000378:metabolism; D010936:Plant Extracts / Q000494:pharmacology*; D026902:Potassium Channel Blockers / Q000494:pharmacology; D011335:Proadifen / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D015220:Calcium Channels; D010936:Plant Extracts; D026902:Potassium Channel Blockers; D011335:Proadifen; D019001:Nitric Oxide Synthase; D002118:Calcium; D008751:Methylene Blue; D019331:NG-Nitroarginine Methyl Ester; D007213:Indomethacin