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

Date Published: April 24, 2019

Publisher: Public Library of Science

Author(s): Suelen Guedes de Oliveira, Erick Roberto Gonçalves Claudio, Simone Alves de Almeida, Vinicius Mengal, Fabricio Bragança da Silva, Nyam Florêncio Silva, Helder Mauad, Glaucia Rodrigues de Abreu, Michael Bader.

http://doi.org/10.1371/journal.pone.0215568

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.

Partial Text

Estrogens play important functions in female organisms, such as the development of sexual organs, cellular proliferation, and bone maturation as well as in the protection of the cardiovascular system [1]. Women in the postmenopausal period become more susceptible to the development of cardiovascular diseases (CVD) such as the myocardial infarction (MI) which stands out because of its high incidence [1].

The aim of the present study was to evaluate the effects of ET on the vascular reactivity and the role of ROS in ovariectomized and infarcted female rats. Therefore, in the vascular reactivity analysis, MI impaired vessel function, exhibited by decreased relaxation and increased contractility. MI is known to trigger the activation of neurohumoral mechanisms, such as the renin-angiotensin-aldosterone system and greater activation of the sympathetic nervous system, which leads to major changes in vessel reactivity [20,21], caused by an imbalance between the release of vasoconstrictor and vasodilatory factors [22]. In accordance, Bianchi et al., 2006 [4] showed that MI increases the vasoconstrictor responses to phenylephrine in aortic rings of ovariectomized rats. Furthermore, acute MI lead to an inflammatory process in which pro-inflammatory cytokines, such as TNF-α, IL-6, and IL-1β, have been identified as the most relevant inflammatory mediators. Sustained high levels of cytokines may trigger endothelial dysfunction [23,24]. Similar studies have shown impairments in vascular reactivity caused by MI in coronary vessels and in mesenteric arteries [25,26]. In aorta arteries, it was reported that MI also has led to impairments in the reactivity only 3 days after the MI induction [27]. In agreement, our results suggest that the changes in the contractility pattern in the infarcted group were mainly promoted by the infarction, and not by the OVX, as the sham group did not differ from the control group.

In conclusion, MI impairs the endothelium-dependent and endothelium-independent vascular reactivity in the aorta of ovariectomized rats, and the increase in oxidative stress through the higher expression of gp91phox contribute to these results. In addition, ET improves vascular reactivity in MI rats by preventing the increase in the expression of gp91phox and the decrease in the enzymatic antioxidant system, resulting in a normal ROS production and the maintenance of NO bioavailability. Thus, ET can be an effective therapeutic strategy for improving the MI-induced vascular alterations in the estrogen deficiency condition.

 

Source:

http://doi.org/10.1371/journal.pone.0215568

 

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