Influence of estrogen on pulmonary arterial hypertension: role of oxidative stress

Siqueira, Rafaela; Carraro, Cristina Campos; Colombo, Rafael; Becker, Cristiano Urbano; Fernandes, Tania Regina Gattelli; Araújo, Alex Sander; Belló‐Klein, Adriane

doi:10.1002/cbf.1784

Cited by 10 publications

(7 citation statements)

References 34 publications

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“…Perhaps, over a longer period, a more prominent increase could be observed, as reported by Konskenvuo et al (2010). This increase in pulmonary pressure seems to be insufficient to induce RV hypertrophy, as was demonstrated in this study, which corroborates previous data from our laboratory (Siqueira et al 2011). This outcome differed from that observed in male rats, where an evident RV hypertrophy was documented (Colombo et al 2013).…”

Section: Discussionsupporting

confidence: 93%

Effects of ovariectomy on antioxidant defence systems in the right ventricle of female rats with pulmonary arterial hypertension induced by monocrotaline

Siqueira

Colombo

Conzatti

et al. 2018

Can. J. Physiol. Pharmacol.

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The aim of this study was to evaluate the impact of ovariectomy on oxidative stress in the right ventricle (RV) of female rats with pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT). Rats were divided into four groups (n=6/group):sham (S), sham + MCT (SM), ovariectomized (O), and ovariectomized + MCT (OM).MCT (60 mg/kg i.p) was injected 1 week after ovariectomy or sham surgery. Three weeks after,, echocardiographic analysis and RV catheterisation were performed. RV morphometric, biochemical, and protein expression analysis through western blotting were done. MCT promoted a slight increase in pulmonary artery pressure, without differences between the SM and OM groups, but did not induce RV hypertrophy. RV hydrogen peroxide increased in the MCT groups, but SOD, CAT, and GPx activities were also enhanced. Non-classical antioxidant defenses diminished in ovariectomized groups, probably due to a decrease in the nuclear factor Nrf2. Hemoxygenase-1 and thioredoxin-1 protein expression was increased in the OM group compared to SM, being accompanied by an elevation in the estrogen receptor β (ER-β). Hemoxygenase-1 and thioredoxin-1 may be involved in the modulation of oxidative stress in the OM group, and this could be responsible for attenuation of PAH and RV remodeling.

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Section: Discussionsupporting

confidence: 93%

Effects of ovariectomy on antioxidant defence systems in the right ventricle of female rats with pulmonary arterial hypertension induced by monocrotaline

Siqueira

Colombo

Conzatti

et al. 2018

Can. J. Physiol. Pharmacol.

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“…38,39 In a study, estrogen levels may help to avoid the appearance of pulmonary edema, the characteristic of MCT model and right ventricular failure. 40 Based on these results, it can be considered that the gender difference found in MCT-induced pulmonary hypertension resulted from higher estrogen levels in female rats than in males.…”

Section: Discussionmentioning

confidence: 96%

The effects of gender difference on monocrotaline-induced pulmonary hypertension in rats

et al. 2013

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The present study aimed to compare the effect of gender difference on hemodynamic consequences in the development of monocrotaline (MCT)-induced pulmonary hypertension in rat. The effect of antioxidant enzyme systems on the development of pulmonary hypertension mediated by the phytotoxin MCT and the effect of gender on these antioxidant systems were also investigated. For this purpose, the right ventricular pressures (RVPs) and right ventricular/heart weight (HW) ratios were compared between groups and the glutathione (GSH) level and superoxide dismutase (SOD), catalase (CAT) and glutathione-S-transferase (GST) activities were determined in lung and liver tissue samples of rats. RVP and right ventricular/HW ratios significantly increased in the MCT group compared to the control group. In the MCT group, RVP was significantly higher in males than females. MCT-induced pulmonary hypertension resulted in decreased GSH level, decreased GST and SOD activities and increased CAT activity in lung and liver tissues of both male and female rats. In addition, the lung and liver GSH level and GST and SOD levels were higher in female control rats compared to male control rats. The results of the present study, that antioxidant enzyme activities were different between the groups, highlight the possible role of oxidative stress in the pathogenesis of MCT-induced pulmonary hypertension in rats. Moreover, the lower antioxidant defense capacity of male rats than female rats may be considered as a cause of more aggressive course of MCT-induced pulmonary hypertension in males compared to females.

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“…Indeed, a growing body of studies has demonstrated that estrogen can act as an antioxidant to regulate cardiovascular function. 34–37 In a spontaneous hypertensive rat model, ovariectomy increased ROS excretion in females, suggesting that estrogen suppresses levels of ROS. 38 In contrast to our previous findings that perinatal nicotine enhances vascular NADPH oxidase (Nox2) protein expression in male adult offspring, 28 current findings that nicotine had no effect on Nox2 expression in female offspring, suggest a sex difference in nicotine-induced programming of ROS-related gene expression.…”

Section: Discussionmentioning

confidence: 99%

Estrogen Normalizes Perinatal Nicotine–Induced Hypertensive Responses in Adult Female Rat Offspring

Xiao

Huang²,

Yang³

et al. 2013

Hypertension

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Perinatal nicotine exposure caused a gender-dependent heightened vascular response to angiotensin II (Ang II) and increased blood pressure in adult male but not female rat offspring. The present study tested the hypothesis that estrogen normalizes perinatal nicotine-induced hypertensive response to Ang II in female offspring. Nicotine was administered to pregnant rats via subcutaneous osmotic minipumps from day 4 of gestation to day 10 after birth. Ovariectomy (OVX) and 17β-estradiol (E2) replacement were performed at 8 weeks old female offspring. At 5 months old, Ang II-induced blood pressure (BP) responses were not changed by nicotine treatment in the sham groups. In contrast, nicotine significantly enhanced Ang II-induced BP responses as compared with saline control in the OVX groups, which was associated with increased Ang II-induced vascular contractions. These heightened responses were abrogated by E2 replacement. In addition, nicotine enhanced Ang II receptor type I (AT1R), NADPH oxidase type 2 (Nox2) protein expressions, and reactive oxygen species (ROS) production of aortas as compared with saline control in the OVX groups. Anti-oxidative agents, both apocynin and tempol, inhibited Ang II-induced vascular contraction and eliminated the differences of contractions between nicotine-treated and control OVX rats. These findings support a key role of estrogen in the sex difference of perinatal nicotine-induced programming of vascular dysfunction, and suggest that estrogen may counteract heightened reactive oxygen species production, leading to protection of females from development programming of hypertensive phenotype in adulthood.

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Influence of estrogen on pulmonary arterial hypertension: role of oxidative stress

Cited by 10 publications

References 34 publications

Effects of ovariectomy on antioxidant defence systems in the right ventricle of female rats with pulmonary arterial hypertension induced by monocrotaline

Effects of ovariectomy on antioxidant defence systems in the right ventricle of female rats with pulmonary arterial hypertension induced by monocrotaline

The effects of gender difference on monocrotaline-induced pulmonary hypertension in rats

Estrogen Normalizes Perinatal Nicotine–Induced Hypertensive Responses in Adult Female Rat Offspring

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