title: Mechanisms of phytoestrogen biochanin A-induced vasorelaxation in renovascular hypertensive rats.
abstract: 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 (ω)-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 Ca(2+)-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.
  
  
  CONCLUSIONS
  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 endothelium-derived activation of voltage-dependent K(+) channels contributes, at least in part, to the relaxant effect of biochanin A in renovascular hypertension.
authors.affiliation: Department of Physiology, College of Medicine, Chosun University, Gwangju, Korea.
authors.forename: Seok
authors.initials: S
authors.lastname: Choi
authors.affiliation: Department of Emergency Medicine, College of Medicine, Chosun University, Gwangju, Korea.
authors.forename: Won Suk
authors.initials: WS
authors.lastname: Jung
authors.affiliation: Department of Emergency Medicine, College of Medicine, Chosun University, Gwangju, Korea.
authors.forename: Nam Soo
authors.initials: NS
authors.lastname: Cho
authors.affiliation: Department of Physiology, College of Medicine, Chosun University, Gwangju, Korea.
authors.forename: Kwon Ho
authors.initials: KH
authors.lastname: Ryu
authors.affiliation: Department of Physiology, College of Medicine, Chosun University, Gwangju, Korea.
authors.forename: Jae Yeoul
authors.initials: JY
authors.lastname: Jun
authors.affiliation: Department of Internal Medicine, College of Medicine, Chosun University, Gwangju, Korea.
authors.forename: Byung Chul
authors.initials: BC
authors.lastname: Shin
authors.affiliation: Department of Internal Medicine, College of Medicine, Chosun University, Gwangju, Korea.
authors.forename: Jong Hoon
authors.initials: JH
authors.lastname: Chung
authors.affiliation: Department of Physiology, College of Medicine, Chosun University, Gwangju, Korea.
authors.forename: Cheol Ho
authors.initials: CH
authors.lastname: Yeum
keywords: Biochanin A; Endothelium; K+ channels; Renovascular hypertension