Other study, it was demonstrated that an increase in collagen deposition contributes to ventricular chamber strain enhancement and compliance reduction. Therefore, collagen reduction plays a key role in reducing adverse remodeling after MI, and participates in the normal distribution of contraction force during the cardiac cycle. The activation of the neurohumoral cascade, as previously described, exerts many adverse effects after MI, including cardiac hypertrophy. These effects have been demonstrated by studies showing that the increases in AT1 receptor expression and AngII after MI, as well as ovarian hormone reduction, increase the expression of endothelin receptor type B, resulting in myocardial hypertrophy. Moreover, the overexpression of AT1 receptors in fibroblasts of adult rats induces hypertrophy and remodeling. Estrogen deficiency didn’t seems to play an important role in this process, because it was not detected difference in cross sectional area and in the AT1 receptor expression between the ovariectomized and control groups. However, it was been previously reported that 14 / 18 Exercise and Myocardial Infarction in OVX Rats the lack of estradiol increases the density of this receptor in rats. Nevertheless, other factors may also contribute to these effects, such as oxidative stress. Oxidative stress is defined as an imbalance between pro- and antioxidant systems, an imbalance that favors the former and causes cellular damage via an increase in ROS formation. After MI, ROS production is markedly enhanced, as showed by DHE fluorescence. NADPH NOD-IN-1 biological activity oxidase is one of the main sources of superoxide production. This complex possesses two membrane bound subunits, as well as more cytosolic subunits which MELK-8a (hydrochloride) web regulate and organize the complex in the membrane, enhancing its activity and producing superoxide. In the heart, Gp91phox plays a key role in remodeling after MI. It has been previously demonstrated that the activation of the AT1 receptor induces an enhancement in superoxide production by NADPH oxidase, causing hypertrophy by a mechanism dependent on Akt and Rac-1 in conjunction with Gp91phox activation. Moreover, the pro-fibrotic effect triggered by the AT1 receptor has been shown to be mediated by Gp91phox. Observations made by Yung et al., illustrate that ovarian hormone deficiency increases ACE, AT1 receptor, Gp91phox and p22phox expression, as well as plasmatic AngII concentrations, events followed by an enhancement in oxidative stress and a reduction in nitric oxide bioavailability. It is important to note that estrogens are antioxidant compounds, and their reduction contributes to ROS elevation, an additional problematic effect of MI. In our study, ET decreases Gp91phox expression in OVX+IMET animals, and this reduction was accompanied by a reduction in collagen deposition and myocyte hypertrophy. A study conducted by Barbosa et al., showed that obese rats subjected to 8 weeks of ET demonstrated reduced superoxide production in parallel with increases in SOD and glutathione peroxidase activity. Similar results were observed by Pinho et al., showing that different training protocols were efficient in decreasing superoxide production in male rats after MI. Antioxidant enzymes play a key role in ROS homeostasis. We also demonstrated that in addition to Gp91phox reduction, there were improvements in the enzymatic antioxidant system in the PubMed 
ID:http://jpet.aspetjournals.org/content/12/2/59 setting of ET, as demonstrated by the increase in catalase expression. In a recent study, we de.Other study, it was demonstrated that an increase in collagen deposition contributes to ventricular chamber strain enhancement and compliance reduction. Therefore, collagen reduction plays a key role in reducing adverse remodeling after MI, and participates in the normal distribution of contraction force during the cardiac cycle. The activation of the neurohumoral cascade, as previously described, exerts many adverse effects after MI, including cardiac hypertrophy. These effects have been demonstrated by studies showing that the increases in AT1 receptor expression and AngII after MI, as well as ovarian hormone reduction, increase the expression of endothelin receptor type B, resulting in myocardial hypertrophy. Moreover, the overexpression of AT1 receptors in fibroblasts of adult rats induces hypertrophy and remodeling. Estrogen deficiency didn’t seems to play an important role in this process, because it was not detected difference in cross sectional area and in the AT1 receptor expression between the ovariectomized and control groups. However, it was been previously reported that 14 / 18 Exercise and Myocardial Infarction in OVX Rats the lack of estradiol increases the density of this receptor in rats. Nevertheless, other factors may also contribute to these effects, such as oxidative stress. Oxidative stress is defined as an imbalance between pro- and antioxidant systems, an imbalance that favors the former and causes cellular damage via an increase in ROS formation. After MI, ROS production is markedly enhanced, as showed by DHE fluorescence. NADPH oxidase is one of the main sources of superoxide production. This complex possesses two membrane bound subunits, as well as more cytosolic subunits which regulate and organize the complex in the membrane, enhancing its activity and producing superoxide. In the heart, Gp91phox plays a key role in remodeling after MI. It has been previously demonstrated that the activation of the AT1 receptor induces an enhancement in superoxide production by NADPH oxidase, causing hypertrophy by a mechanism dependent on Akt and Rac-1 in conjunction with Gp91phox activation. Moreover, the pro-fibrotic effect triggered by the AT1 receptor has been shown to be mediated by Gp91phox. Observations made by Yung et al., illustrate that ovarian hormone 
deficiency increases ACE, AT1 receptor, Gp91phox and p22phox expression, as well as plasmatic AngII concentrations, events followed by an enhancement in oxidative stress and a reduction in nitric oxide bioavailability. It is important to note that estrogens are antioxidant compounds, and their reduction contributes to ROS elevation, an additional problematic effect of MI. In our study, ET decreases Gp91phox expression in OVX+IMET animals, and this reduction was accompanied by a reduction in collagen deposition and myocyte hypertrophy. A study conducted by Barbosa et al., showed that obese rats subjected to 8 weeks of ET demonstrated reduced superoxide production in parallel with increases in SOD and glutathione peroxidase activity. Similar results were observed by Pinho et al., showing that different training protocols were efficient in decreasing superoxide production in male rats after MI. Antioxidant enzymes play a key role in ROS homeostasis. We also demonstrated that in addition to Gp91phox reduction, there were improvements in the enzymatic antioxidant system in the PubMed ID:http://jpet.aspetjournals.org/content/12/2/59 setting of ET, as demonstrated by the increase in catalase expression. In a recent study, we de.
