Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/16191
Title: Analysis of the mechanisms underlying the endothelium-dependent antivasoconstriction of puerarin in rat aorta
Authors: Yan, LP
Zhuang, YL
Chan, SW
Chen, SL
Shi, GG
Keywords: Antivasoconstriction
Ca 2+ influx
K + channel
NO/NO-cGMP
Puerarin
Rat aorta
Issue Date: 2009
Publisher: Springer
Source: Naunyn-schmiedeberg's archives of pharmacology, 2009, v. 379, no. 6, p. 587-597 How to cite?
Journal: Naunyn-Schmiedeberg's Archives of Pharmacology 
Abstract: Puerarin, a major isoflavonoid compound from the Chinese herb, Ge-gen (Pueraria lobata), has effective treatment on myocardial and cerebral ischemia, glaucoma and sudden deafness in clinical setting in China. Our present work showed that puerarin (50, 150, 450 μM) concentration-dependently inhibited phenylephrine or KCl-induced contraction only in endothelium-intact rat aortic rings. In Ca 2+-free solution, the antivasoconstriction of puerarin on phenylephrine was totally deprived. N G-nitro-l-arginine methyl ester, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, indomethacin and the three K + channel blockers, glibenclamide, tetraethylammonium and Ba 2+ displayed significant inhibitory effects on the antivasoconstriction of puerarin. 8-bromo-cGMP significantly strengthened the action of puerarin. Puerarin (10-160 μM) concentration-dependently induced the NO production in the rat aortic cells. These findings suggested that the antivasoconstriction elicited by puerarin is endothelium-dependent. NO/NO-cGMP pathway, PGI 2 and the opening of K + channels sensitive to glibenclamide, tetraethylammonium, and Ba 2+, which might be triggered by the extracellular Ca 2+ influx in the endothelium, appear to contribute to the antivasoconstriction of puerarin.
URI: http://hdl.handle.net/10397/16191
DOI: 10.1007/s00210-008-0388-2
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