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Mechanism of glabridin‐mediated vasorelaxation of rat main mesenteric artery
Author(s) -
Aaronson Philip,
Chanda Debrabata
Publication year - 2013
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.27.1_supplement.1092.5
Subject(s) - myograph , chemistry , glibenclamide , hyperpolarization (physics) , mesenteric arteries , vasodilation , biophysics , vascular smooth muscle , electrical impedance myography , pharmacology , medicine , smooth muscle , endocrinology , artery , biology , stereochemistry , nuclear magnetic resonance spectroscopy , diabetes mellitus
Glabridin is one of the major flavonoids found in Glycyrrhiza glabra (licorice) root, an important traditional Chinese medicine, and has been reported to have anti‐atherogenic, anti‐inflammatory and anti‐nephritic properties. Because its acute effect on vascular tone remains unknown, we examined whether glabridin was able to relax rat main mesenteric arteries (RMMA) which had been preconstricted with norepinephrine or U46619. RMMA were mounted on a Mulvany‐Halpern type myograph and isometric tension development was monitored. Glabridin caused a relaxation of preconstricted RMMA at a concentration of as little as 0.1 μM, with a relaxation of ~70% being recorded at a concentration of 30 μM. Relaxation was endothelium‐independent, and was strongly inhibited if the K + concentration in the bathing solution was raised to 20 mM. Relaxation was also strongly antagonized by inhibiting BK Ca channels (with 1 mM TEA), K V channels (with 300 μM 4‐AP), or K ATP channels (with 10 μM glibenclamide). These results indicate that glabridin, in a concentration range relevant to that which it may attain in plasma in vivo, induces a vasorelaxation which requires vascular smooth muscle hyperpolarization, possibly mediated by the opening of several types of K + channels.