KMID : 0359920140330040181
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Korean Journal of Nephrology 2014 Volume.33 No. 4 p.181 ~ p.186
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Mechanisms of phytoestrogen biochanin A-induced vasorelaxation in renovascular hypertensive rats
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Choi Seok
Jung Won-Suk Cho Nam-Soo Ryu Kwon-Ho Jun Jae-Yeoul Shin Byung-Chul Chung Jong-Hoon Yeum Cheol-Ho
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Abstract
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Background: The plant-derived estrogen biochanin A is known to cause vasodilation, but its mechanism of action in hypertension remains unclear. This study was undertaken to investigate the effects and mechanisms of biochanin A on the thoracic aorta in two-kidney, one clip (2K1C) renovascular hypertensive rats.
Methods: Hypertension was induced by clipping the left renal artery, and control age-matched rats were sham treated. Thoracic aortae were mounted in tissue baths to measure isometric tension.
Results: Biochanin A caused concentration-dependent relaxation in aortic rings from 2K1C hypertensive and sham-treated rats, which was greater in 2K1C rats than in sham rats. Biochanin A-induced relaxation was significantly attenuated by
removing the endothelium in aortic rings from 2K1C rats, but not in sham rats. N¥ø-Nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, or indomethacin, a cyclooxygenase inhibitor, did not affect the biochanin A-induced relaxation in
aortic rings from 2K1C and sham rats. By contrast, treatment with glibenclamide, a selective inhibitor of adenosine triphosphate-sensitive K© channels, or tetraethylammonium, an inhibitor of Ca2©-activated K© channels, significantly reduced biochanin A-induced relaxation in aortic rings from both groups. However, 4-aminopyridine, a selective inhibitor of voltage-dependent K© channels, inhibited the relaxation induced by biochanin A in 2K1C rats, whereas no significant
differences were observed in sham rats.
Conclusion: These results suggest that the enhanced relaxation caused by biochanin A in aortic rings from hypertensive rats is endothelium dependent. Vascular smooth muscle K© channels may be involved in biochanin A-induced relaxation in aortae from hypertensive and normotensive rats. In addition, an endotheliumderived activation of voltage-dependent K© channels contributes, at least in part, to the relaxant effect of biochanin A in renovascular hypertension.
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KEYWORD
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Biochanin A, Endothelium, K© channels, Renovascular hypertension
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