Exercise training improves vascular reactivity in ovariectomized rats subjected to myocardial infarction

PLoS One. 2019 Apr 24;14(4):e0215568. doi: 10.1371/journal.pone.0215568. eCollection 2019.

Abstract

The aim of this study was to evaluate the effects of exercise training (ET) on the aortic vascular reactivity of ovariectomized and infarcted rats. The animals were divided into 5 groups: Control, Ovariectomized + SHAM sedentary (OVX+SHAMSED), OVX+SHAM and ET (OVX+SHAMET), OVX + Myocardial Infarction sedentary (OVX+MISED), and OVX + MI and ET (OVX+MIET). ET protocol (60 minutes/day, 5x/week) in a motorized treadmill began 15 days after MI and lasted 8 weeks. The endothelium-dependent and endothelium-independent vascular reactivity were evaluated as well as the role of the reactive oxygen species (ROS). Superoxide and nitric oxide (NO) production were analyzed in situ using DHE and DAF-2 fluorescence, respectively. The expression of gp91phox and of the antioxidant enzymes were evaluated by western blotting in the thoracic aorta samples. MI promoted a significant increase in the contractile response and impaired endothelium-mediated relaxation. However, ET prevented the impairment in the vascular reactivity in MI animals. In addition, the protein expression of gp91phox and superoxide production increased and the NO production decreased in the OVX+MISED group but not in the OVX+MIET group. Therefore, ET improves vascular reactivity in MI ovariectomized rats by preventing the increase in the expression of gp91phox and the decrease in the antioxidant enzymes, resulting in a normal ROS and NO production. Thus, ET can be an effective therapeutic strategy for improving the MI-induced vascular alterations in estrogen deficiency condition.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants / metabolism
  • Aorta, Thoracic / physiopathology
  • Endothelium, Vascular / physiopathology
  • Estrogens / deficiency
  • Female
  • Myocardial Infarction / etiology
  • Myocardial Infarction / physiopathology
  • Myocardial Infarction / therapy*
  • NADPH Oxidase 2 / metabolism
  • Nitric Oxide / metabolism
  • Ovariectomy / adverse effects*
  • Oxidative Stress
  • Physical Conditioning, Animal*
  • Rats
  • Rats, Wistar
  • Reactive Oxygen Species / metabolism
  • Superoxides / metabolism
  • Vasodilation / physiology

Substances

  • Antioxidants
  • Estrogens
  • Reactive Oxygen Species
  • Superoxides
  • Nitric Oxide
  • Cybb protein, rat
  • NADPH Oxidase 2

Grants and funding

This study was funded by the Fundação de Amparo a Pesquisa do Espírito Santo (FAPES), process number 67659764/2014, and by the Conselho Nacional de Desenvolvimento Científico e Técnológico (CNPq), process number 443409/2014-5 to GRdA.