title: Myocardial infarction increases reactivity to phenylephrine in isolated aortic rings of ovariectomized rats.
abstract: Clinical studies demonstrated that the incidence of cardiovascular disease is low in premenopausal women, rises in postmenopausal women, and is reduced to premenopausal levels in postmenopausal women who receive estrogen therapy. The interaction between gender and myocardial infarction indicates that the survival advantage of women is modified by the occurrence of myocardial infarction. Therefore, the effect of myocardial infarction on mortality is greater in women than men. The aim of our study was to investigate the influence of the ovariectomy on the reactivity to phenylephrine in aortic rings of female rats post-myocardial infarction. Animals were divided in four groups: Control (Cont), Ovariectomized (Ovx), Infarcted (Inf) and Ovariectomized and Infarcted (Ovx-Inf). Aortic rings were studied 60 days after ovariectomy and infarction surgery. The infarct area was similar among groups. The maximal response to phenylephrine was increased in the Ovx-Inf group compared to all the other groups (Cont = 2.411+/-0.131 (N = 11); Ovx = 2.863+/-0.121(N = 15); Inf = 2.794+/-0.102 (N = 13); Ovx-Inf = 3.40+/-0.201* (N = 12) g; *P < 0.05). In the absence of endothelium and L-NAME perfusion, the maximal response to phenylephrine was similarly increased in all groups. Relaxation to acetylcholine was also similar. The indirect evaluation of NO bioavailability analyzed by the area under the curve demonstrated a reduction on NO on the Ovx-Inf group that could contributes to increased response to phenylephrine. In conclusion our results showed that ovariectomy associated to a myocardial infarction leads to an increment of aorta reactivity to phenylephrine associated to a reduction of basal NO bioavailability in spite of a normal endothelium-dependent relaxation induced by acetylcholine.
authors.affiliation: Department of Physiological Sciences, Federal University of Espirito Santo, Av. Marechal Campos, 1468, CEP 29040-090, Vitória, ES, Brazil.
authors.forename: Patrícia Rocon
authors.initials: PR
authors.lastname: Bianchi
authors.forename: Brenda Pires
authors.initials: BP
authors.lastname: Gumz
authors.forename: Karina
authors.initials: K
authors.lastname: Giuberti
authors.forename: Ivanita
authors.initials: I
authors.lastname: Stefanon
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects* / Q000473:pathology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004338:Drug Combinations; D004730:Endothelium, Vascular / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D005260:Female; D066298:In Vitro Techniques; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D010052:Ovariectomy; D010656:Phenylephrine / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D004338:Drug Combinations; D014662:Vasoconstrictor Agents; D010656:Phenylephrine; D009569:Nitric Oxide; D019331:NG-Nitroarginine Methyl Ester