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An aqueous extract of Lespedeza cuneata dilates vascular smooth muscle via endothelium‐dependent NO/cGMP signaling
Author(s) -
Lee Jun Kyoung,
Cao Li Hua,
Kang Dae Gill,
Yang Sun Nye,
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-a
Subject(s) - tetraethylammonium , phenylephrine , vascular smooth muscle , chemistry , glibenclamide , vasodilation , verapamil , pharmacology , endothelium , apamin , atropine , thoracic aorta , endocrinology , medicine , aorta , potassium channel , smooth muscle , potassium , calcium , blood pressure , organic chemistry , diabetes mellitus
The aqueous extract of Lespedeza cuneata G. Don (ALC) induced vascular relaxation of the phenylephrine‐precontracted aorta in a dose dependent manner, which was abolished by removal of functional endothelium. Pretreatment of the aortic tissues with N G ‐nitro‐L‐arginine methyl ester (L‐NAME) and 1H‐[1,2,4]‐oxadiazole‐[4,3‐α]‐quinoxalin‐1‐one (ODQ) inhibited the vascular relaxation induced by ALC, respectively. ALC‐induced vascular relaxation was also markedly attenuated by addition of verapamil or diltiazem, while the relaxant effect of ALC was not blocked by pretreatment with indomethacine, glibenclamide, tetraethylammonium (TEA), atropine, and propranolol, respectively. Incubation of endothelium‐intact thoracic aortic ring with ALC increased the production of cGMP. However, ALC‐induced cGMP production was blocked by pretreatment with L‐NAME or ODQ. These results suggest that ALC dilates vascular smooth muscle via endothelium‐dependent NO/cGMP signaling.