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Scutellarin‐induced endothelium‐independent relaxation in rat aorta
Author(s) -
Pan Zhenwei,
Feng Tieming,
Shan Luchen,
Cai Benzhi,
Chu Wenfeng,
Niu Huili,
Lu Yanjie,
Yang Baofeng
Publication year - 2008
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.2364
Subject(s) - scutellarin , verapamil , chemistry , pharmacology , calcium , tetraethylammonium , potassium channel , calcium channel , endocrinology , medicine , potassium , organic chemistry
Scutellarin is a flavonoid extracted from the traditional Chinese herb, Erigeron breviscapus Hand Mazz. In the present study, the vasorelaxant effects of scutellarin and the underlying mechanism were investigated in isolated rat aorta. Scutellarin (3, 10, 30, 100 µ m ) caused a dose‐dependent relaxation in both endothelium‐intact and endothelium‐denuded rat aortic rings precontracted with noradrenaline bitartrate (IC 50 = 7.7 ± 0.6 µ m ), but not with potassium chloride. Tetraethylammonium, glibenclamide, atropine, propranolol, indomethacin and N(G)‐nitro‐ l ‐arginine methyl ester had no influence on the vasorelaxant effect of scutellarin, which further excluded the involvement of potassium channels, muscarinic receptor, nitric oxide pathway and prostaglandin in this effect. Pretreatment with scutellarin decreased the tonic phase, but not the phasic phase of the noradrenaline bitartrate induced tension increment. Scutellarin also alleviated Ca 2+ ‐induced vasoconstriction in Ca 2+ ‐depleted/noradrenaline bitartrate pretreated rings in the presence of voltage‐dependent calcium channel blocker verapamil. The noradrenaline bitartrate evoked intracellular calcium increase was inhibited by scutellarin. Scutellarin had no effect on phorbol‐12,13‐diacetate induced contraction in a calcium‐free bath solution. These results showed that scutellarin could relax thoracic artery rings in an endothelium‐independent manner. The mechanism seems to be the inhibition of extracellular calcium influx independent of the voltage‐dependent calcium channel. Copyright © 2008 John Wiley & Sons, Ltd.