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Hypotensive Effect of Crotalaria Sessiliflora L. Extract in In‐vivo and In‐vitro Approaches
Author(s) -
Koh Sang Bum,
Kang Myung Hwa,
Kim Tae Su,
Cho Young Min,
Seong Ha Jung,
Park Cheol Beom,
Seong Yeon Hee
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.a1086-a
The aim of the present study is to investigate the hypotensive effect of Crotalaria sessiliflora L. extract (CSE) on rats and its mechanism when combining in‐vivo and in‐vitro approaches. CSE induced a concentration‐dependent relaxation on endothelium‐intact thoracic aortic rings precontracted with phenylephrine (PE). Pretreatment of the aortic strips with either NG‐nitro‐L‐arginine (L‐NNA) or methylene blue significantly reduced the relaxation induced by CSE. CSE increased the production of cGMP in endothelium‐intact aortic rings and this effect was significantly attenuated by L‐NNA and methylene blue. Relaxation in response to CSE in strips precontracted with PGF2a was eliminated by removing extracellular Ca2+ and significantly reduced by the pretreatment with ruthenium red. This vasorelaxant effect of CSE was markedly reduced by tetraethylammonium (TEA) but not affected by verapamil and tolbutamide. The vasorelaxant effect of CSE in PE‐precontracted aortic strips was completely inhibited by atropine but not by diphenhydramine and propranolol. The hypotensive response induced by CSE was completely abolished by atropine and significantly attenuated by L‐NNA in conscious unrestrained SHRs. Therefore, it is concluded that CSE causes vasorelaxation mediated by NO generation through M3 receptor activation in in‐vivo as well as in in‐vitro. These findings may provide the pharmacological basis of the clinical usage of CSE in treatment of hypertension.