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Trifolirhizin and desmethylicaritin, active components of roots of Sophora flavescens AIT., induced vascular relaxation via NO/cGMP signaling
Author(s) -
Kang Dae Gill,
Lee Xiang,
Lee Jun Kyoung,
Choi Deok Ho,
Chai Kyu Yun,
Lee Ho Sub
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1240-b
Subject(s) - diltiazem , muscarinic acetylcholine receptor , sophora flavescens , verapamil , chemistry , pharmacology , phenylephrine , vascular smooth muscle , atropine , vasodilation , endothelium , receptor , endocrinology , medicine , biochemistry , calcium , smooth muscle , matrine , chromatography , blood pressure
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 N G ‐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 Ca 2+ 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