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  • Title: Endothelium-dependent and direct relaxation induced by ethyl acetate extract from Flos Chrysanthemi in rat thoracic aorta.
    Author: Jiang HD, Cai J, Xu JH, Zhou XM, Xia Q.
    Journal: J Ethnopharmacol; 2005 Oct 03; 101(1-3):221-6. PubMed ID: 15950416.
    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.
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