| Objective: Equol, an isoflavonoid metabolite produced from the dietary isoflavone daidzein. The aim was to evaluate the effects of equol on the cardiovascular system. (1) To investigate the vascular response of equol on isolated rat aortic rings and its possible mechanisms. (2) To investigate the effects of equol on the myocardial ischemia/reperfusion injury.Methods: (1) The method of recording the isometric force in the isolated thoracic aorta rings was used to evaluate the effects of equol on the rings and whether endothelium-derived relaxing factors(EDRF), K+ channels and Ca2+ channels were involved in the action of equol. (2) Isolated rat hearts were perfused in Langendorff apparatus. The hearts were subjected to 30min regional ischemia and 180min reperfusion by ligating and relaxing the left anterior descending coronary arteries(LAD). Various concentrations of equol were administrated before ischemia for 10 min. Infarct size, creatine kinase (CK) release and ventricular hemodynamic parameters (HR,LVDP,+dp/dtmax and -dp/dtmax) were measured.Results: (1) Equol markedly relaxed aortic rings pre-contracted with phenylephrine(PE, 1×10-6 mol/L ) or KCl (6×10-2 mol/L) in a dose-dependent manner, but had no effect on the basic tesion. The vasorelaxant potency of equol was attenuated by the removal of the endothelium. The vasorelaxant effect of equol in endothelium-intact rings was significantly reduced by pretreatment with L-NAME(1×10-4mol/L), an inhibitor of NOS, and methylene blue(1×10-5mol/L), an inhibitor of guanylyl cyclase . However, indomethacin(1×10-5mol/L), a cyclooxygenase blocker, did not significantly affect the vasodilation of equol. 4-Aminopyridine(1×10-2mol/L), a non-specific K+ channel blocker, inhibited relaxation of equol in endothelium-denuded rings precontracted by PE. Equol also significantly reduced contraction induced by increasing external calcium in Ca2+-free medium plus 6×10-2 mol/L KCl. Moreover, equol markedly inhibited a Ca2+ -channel agonist Bay K8644-induced contraction in endothelium-denuded rings. (2) Compared with sham group, myocardial ischemia/reperfusion caused irreversible injury in the isolated hearts model. Administration of equol could not reduce the infarct size, CK release and improve the left ventricular function (LVDP,+dp/dtmax and -dp/dtmax).Conclusion: (1) Our results suggest that equol induces relaxation in rat aortic rings through both endothelium-dependent and -independent mechanisms. The vasorelaxant effect of equol is partially mediated by NO-cGMP pathway and independent of prostanoid . Opening K+ channels and blocking Ca2+ channels in the vascular muscle cells are also involved in the relaxation of equol. (2) The findings indicate that equol does not affect the infarct size, CK release and the left ventricular performance induced by ischemia/reperfusion injury in the isolated rat hearts . So there is no evidence that equol has cadioprotective effects against myocardial ischemia/reperfusion injury. |
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