The Effect of Eqoul, a Metabolite of Isoflavone, on Endothelial Cell-independent Vasodilatation of Human Uterine Artery In Vitro.
10.11005/jbm.2015.22.2.57
- Author:
Jeong Yuen KIM
1
;
Moo Yeol LEE
;
Hyoung Moo PARK
Author Information
1. Department of Obstetrics and Gynecology, Chung-Ang University College of Medicine, Seoul, Korea. hmpark52@hanmail.net
- Publication Type:In Vitro ; Original Article
- Keywords:
Equol;
Vasodilation;
Mucsle smooth
- MeSH:
Calcium;
Cell Membrane;
Equol;
Female;
Humans;
Hysterectomy;
Muscle, Smooth;
Muscle, Smooth, Vascular;
Phenylephrine;
Phytoestrogens;
Relaxation;
Uterine Artery*;
Vasodilation*
- From:Journal of Bone Metabolism
2015;22(2):57-69
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: The purpose of this study is to investigate 1) whether equol has the direct modulation on vascular tone of endothelium-denuded human uterine artery, and 2) if present, whether this equol-induced modulation of vascular tone is mediated by intracellular calcium modulation through Ca2+ & K+ channels on vascular smooth muscle cell membrane. METHODS: The uterine arteries were obtained at the time of hysterectomy from 15 women. The uterine smooth muscles were pretreated with phenylephrine, 10(-5) M & high KCl solution 70 mM. The equol at 6 different concentrations from 10(-11) to 10(-6) M were used for the evaluation of modulatory action of equol on precontracted vascular smooth. The cumulative concentration-response for equol were determined on phenylephrine-induced contractions and compared with the results without pretreatment. RESULTS: Equol 10(-11) to 10(-6) M in concentration showed relaxation effect on vascular smooth muscle contraction which was induced by phenylephrine 10(-5) M. This relaxation effect of equol was dose-dependent. Equol in same concentrations showed no significant effects on vascular smooth muscle contraction induced by high KCI solution. Phenylephrine-induced contraction was markedly reduced from 10(-7) to 10(-4) M in concentration by pretreatment of equol, but high KCI-induced contraction was not affected by pretreatment of equol. CONCLUSIONS: This vasodilatation effect of equol may be induced by calcium antagonistic action, which was mediated through antagonistic action for receptor-dependent Ca2+ channel, but not for voltage-dependent Ca2+ channel. As far as we know, this is the first report of phytoestrogen equol on vascular reactivity of human vessels.
