Mechanisms of phytoestrogen biochanin A-induced vasorelaxation in renovascular hypertensive rats.
10.1016/j.krcp.2014.08.003
- Author:
Seok CHOI
1
;
Won Suk JUNG
;
Nam Soo CHO
;
Kwon Ho RYU
;
Jae Yeoul JUN
;
Byung Chul SHIN
;
Jong Hoon CHUNG
;
Cheol Ho YEUM
Author Information
1. Department of Physiology, College of Medicine, Chosun University, Gwangju, Korea. chyum@chosun.ac.kr
- Publication Type:Original Article
- Keywords:
Biochanin A;
Endothelium;
K+ channels;
Renovascular hypertension
- MeSH:
4-Aminopyridine;
Adenosine;
Animals;
Aorta;
Aorta, Thoracic;
Baths;
Endothelium;
Estrogens;
Glyburide;
Hypertension;
Hypertension, Renovascular;
Indomethacin;
Muscle, Smooth, Vascular;
Nitric Oxide Synthase;
Phytoestrogens*;
Potassium Channels, Calcium-Activated;
Prostaglandin-Endoperoxide Synthases;
Rats*;
Relaxation;
Renal Artery;
Vasodilation*
- From:Kidney Research and Clinical Practice
2014;33(4):181-186
- CountryRepublic of Korea
- Language:English
-
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. Nomega-Nitro-L-arginine methylester, 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, ortetraethy-lammonium, 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 endothelium-derived activation of voltage-dependent K+ channels contributes, at least in part, to the relaxant effect of biochanin A in renovascular hypertension.
