title: Vasorelaxant and antioxidant activity of the isoflavone metabolite equol in carotid and cerebral arteries.
abstract: OBJECTIVE
  Equol is the main active intestinal metabolite of the isoflavone daidzein and is postulated to be responsible for the cardiovascular benefits of soy. Cerebral vascular effects of equol are unknown. We compared the vasorelaxant and antioxidant effects of equol and daidzein in carotid and basilar artery of normal and hypertensive rats.
  
  
  METHODS
  Relaxant responses to equol and daidzein were measured in the isolated carotid artery and in the basilar artery in vivo. Effects of nitric oxide synthase (NOS) inhibition, high extracellular K(+), endothelial removal and gender on responses to equol were investigated in carotid arteries. Antioxidant activity was assessed as the reduction of NADPH-induced superoxide levels. Hypertension was induced using angiotensin II (0.7 mg/kg per day for 14 days).
  
  
  RESULTS
  In normotensive rats, equol displayed vasorelaxant activity similar to daidzein. The relaxant effect of equol was independent of an intact endothelium, NOS activity, K(+) channels and gender. In the basilar artery, where superoxide levels are higher, equol exerted weak antioxidant effects, whereas effects of daidzein were insignificant. During hypertension, equol-induced vasorelaxation was preserved, whereas relaxant responses to daidzein were impaired.
  
  
  CONCLUSIONS
  Equol possesses substantial vasodilator and weak antioxidant activity in cerebral arteries, with similar activity to daidzein, whereas in hypertension the vasorelaxant response to equol, but not daidzein, is preserved. However, daidzein possesses comparable direct vascular effects with equol, without the need for intestinal conversion to equol. Nevertheless, equol may represent a more useful therapeutic agent during cerebral vascular disease.
authors.affiliation: Department of Pharmacology, The University of Melbourne, Parkville, Victoria, 3010, Australia.
authors.forename: Katherine A
authors.initials: KA
authors.lastname: Jackman
authors.forename: Owen L
authors.initials: OL
authors.lastname: Woodman
authors.forename: Sophocles
authors.initials: S
authors.lastname: Chrissobolis
authors.forename: Christopher G
authors.initials: CG
authors.lastname: Sobey
mesh_terms: D000704:Analysis of Variance; D000804:Angiotensin II; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D002339:Carotid Arteries / Q000187:drug effects*; D002536:Cerebral Arteries / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D004791:Enzyme Inhibitors / Q000494:pharmacology; D060754:Equol; D005260:Female; D006973:Hypertension / Q000139:chemically induced / Q000188:drug therapy / Q000473:pathology; D066298:In Vitro Techniques; D007529:Isoflavones / Q000494:pharmacology*; D008297:Male; D048789:Phytoestrogens / Q000494:pharmacology; D051381:Rats; D013481:Superoxides / Q000378:metabolism; D014664:Vasodilation / Q000187:drug effects
chemical_list: C007610:4',7-dihydroxy-3,4-dihydroisoflavone; D000975:Antioxidants; D004791:Enzyme Inhibitors; D007529:Isoflavones; D048789:Phytoestrogens; D013481:Superoxides; D000804:Angiotensin II; D060754:Equol; C004742:daidzein