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Trifolirhizin and desmethylicaritin, active components of roots of Sophora flavescens AIT., induced vascular relaxation via NO/cGMP signaling

Trifolirihizin and desmethylicaritin isolated from roots of Sophora flavescens Ait. induced relaxation of the phenylephrine‐precontracted aorta in a dose‐dependent manner, respectively, which were disappeared by removal of functional endothelium. Pretreatment of the aortic tissues with NG‐nitro‐L‐ar...

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Bibliographic Details
Published in:The FASEB journal 2007, Vol.21 (6), p.A1240-A1240
Main Authors: Kang, Dae Gill, Lee, Xiang, Lee, Jun Kyoung, Choi, Deok Ho, Chai, Kyu Yun, Lee, Ho Sub
Format: Article
Language:English
Online Access:Get full text
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Summary:Trifolirihizin and desmethylicaritin isolated from roots of Sophora flavescens Ait. induced relaxation of the phenylephrine‐precontracted aorta in a dose‐dependent manner, respectively, which were disappeared by removal of functional endothelium. Pretreatment of the aortic tissues with NG‐nitro‐L‐arginine methylester (L‐NAME), or 1H‐[1,2,4]‐oxadiazole‐[4,3‐¥á]‐quinoxalin‐1‐one (ODQ) inhibited the relaxation induced by trifolirhizin and desmethylicaritin, respectively. Trifolirhizin‐induced relaxations were also markedly attenuated by addition of verapamil, diltiazem, or atropine. Desmethylicaritin‐induced vascular relaxation was also markedly attenuated by addition of verapamil or diltiazem but not by atropine. These results suggest that trifolirhizin dilates vascular smooth muscle via endothelium‐dependent NO/cGMP signaling pathways possible involvement of L‐type Ca2+ channels and/or muscarinic receptor. However, the mechanism of desmethylicaritin‐induced vascular relaxation was dependent on endothelium‐dependent NO/cGMP signaling pathway without involvement of muscarinic receptor
ISSN:0892-6638
1530-6860
DOI:10.1096/fasebj.21.6.A1240-b