Abstract

BackgroundThe 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.MethodsThe 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.ResultsEquol 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.ConclusionsThis 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.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.