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Effect of Lophatherum gracile Brongn on the mechanism of vasorelaxation in thoracic aorta
Author(s) -
Kim Hye Yoom,
Li Xiang,
Kang Dae Gill,
Lee Ho Sub
Publication year - 2010
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.24.1_supplement.986.15
Subject(s) - verapamil , tetraethylammonium , chemistry , glibenclamide , aorta , endothelium , vasodilation , vascular smooth muscle , thoracic aorta , diltiazem , electrical impedance myography , pharmacology , nitric oxide , endocrinology , medicine , smooth muscle , calcium , potassium , organic chemistry , diabetes mellitus
The vasorelaxant effect of an ethanol extract of Lophatherum gracile Brongn (ELB) and the possible mechanism were ascertained in aortic tissues isolated from rats. ELB relaxed endothelium‐intact thoracic aorta in a dose‐dependent manner. However, the induced vascular relaxation was abolished by removal in endothelium of the thoracic aorta. Pretreatment of endothelium‐intact vascular tissues with N G ‐nitro‐L‐arginine methyl ester (L‐NAME) or 1H‐[1,2,4]‐oxadiazole‐[4,3‐¥á]‐quinoxalin‐1‐one (ODQ) significantly inhibited vascular relaxation induced by ELB. Moreover, ELB significantly increased cGMP production in aortic tissues, which was blocked by pretreatment with L‐NAME or ODQ. The vasorelaxant effect of ELB was attenuated by tetraethylammonium (TEA), and glibenclamide. ELB‐induced vasorelaxation was not blocked by atropine, propranolol, indomethacin, verapamil, and diltiazem. Taken together, the present study demonstrates that ELB dilates vascular smooth muscle via an endothelium‐dependent NO‐cGMP signaling pathway, which may be at least, in part, related with the function of K + channels.