Article Publish Status: FREE
Abstract Title:

Mechanisms of phytoestrogen biochanin A-induced vasorelaxation in renovascular hypertensive rats.

Abstract Source:

Kidney Res Clin Pract. 2014 Dec ;33(4):181-6. Epub 2014 Nov 12. PMID: 26885474

Abstract Author(s):

Seok Choi, Won Suk Jung, Nam Soo Cho, Kwon Ho Ryu, Jae Yeoul Jun, Byung Chul Shin, Jong Hoon Chung, Cheol Ho Yeum

Article Affiliation:

Seok Choi


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 bybiochanin 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.

Study Type : Animal Study
Additional Links
Pharmacological Actions : Vasodilator Agents : CK(347) : AC(74)

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