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Bakuchicin induces Vascular Relaxation via Endothelium‐dependent NO‐ cGMP Signaling
Author(s) -
Li Xiang,
Lee Yun Jung,
Kim Youn Chul,
Jeong Gil Saeng,
Cui Hao Zhen,
Kim Hye Yoom,
Kang Dae Gill,
Lee Ho Sub
Publication year - 2011
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.3478
Subject(s) - verapamil , tetraethylammonium , vasodilation , phenylephrine , glibenclamide , pharmacology , chemistry , nitric oxide , endothelium , diltiazem , endocrinology , medicine , calcium , potassium , diabetes mellitus , organic chemistry , blood pressure
Bakuchicin is a furanocoumarin derived from the seeds of Psoralea corylifolia . The aim of the present study was to investigate the effect of bakuchicin on vascular tone in rat aortic tissue. Bakuchicin induced a dose‐dependent relaxation of phenylephrine‐precontracted rat aorta which was abolished by removal of the endothelium. Pretreatment of the endothelium‐intact aortic tissues with NG‐nitro‐ l ‐arginine methylester (L‐NAME) or 1H‐[1,2,4]‐oxadiazole‐[4,3‐α]‐quinoxalin‐1‐one (ODQ) significantly inhibited the vascular relaxation induced by bakuchicin. Incubation with bakuchicin increased the production of cGMP in a concentration‐dependent manner, and this effect was blocked by pretreatment with both L‐NAME and ODQ. Vascular relaxation induced by bakuchicin was significantly inhibited by pretreatment with verapamil and diltiazem, but not by several other inhibitors including tetraethylammonium (TEA), glibenclamide, indomethacin, atropine or propranolol. These results suggested that bakuchicin‐induced vasodilatation is closely associated with the endothelium‐dependent nitric oxide (NO)/cGMP signaling pathway, with the possible involvement of L‐type Ca 2+ channels. Copyright © 2011 John Wiley & Sons, Ltd.

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