Mechanisms Responsible for Endothelial Dysfunction Associated With Acute Estrogen Deprivation in Normotensive Women

Virdis, Agostino; Ghiadoni, Lorenzo; Pinto, Stefania; Lombardo, M.; Petraglia, Felice; Gennazzani, Andrea; Buralli, Simona; Taddei, Stefano; Salvetti, Antonio

doi:10.1161/01.cir.101.19.2258

Cited by 149 publications

(98 citation statements)

References 54 publications

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“…In humans it has been suggested that the endothelial dysfunction secondary to acute endogenous estrogen deprivation (surgical ovariectomy) is caused by reduced NO availability, which results from COX-dependent production of oxidative stress (39).…”

Section: Oxidative Stress -Reactive Oxygen Speciesmentioning

confidence: 99%

Effects of estrogen on the vascular system

Tostes

Nigro

Fortes

et al. 2003

Braz J Med Biol Res

173

126

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The cardiovascular protective actions of estrogen are partially mediated by a direct effect on the vessel wall. Estrogen is active both on vascular smooth muscle and endothelial cells where functionally competent estrogen receptors have been identified. Estrogen administration promotes vasodilation in humans and in experimental animals, in part by stimulating prostacyclin and nitric oxide synthesis, as well as by decreasing the production of vasoconstrictor agents such as cyclooxygenase-derived products, reactive oxygen species, angiotensin II, and endothelin-1. In vitro, estrogen exerts a direct inhibitory effect on smooth muscle by activating potassium efflux and by inhibiting calcium influx. In addition, estrogen inhibits vascular smooth muscle cell proliferation. In vivo, 17ß-estradiol prevents neointimal thickening after balloon injury and also ameliorates the lesions occurring in atherosclerotic conditions. As is the case for other steroids, the effect of estrogen on the vessel wall has a rapid non-genomic component involving membrane phenomena, such as alteration of membrane ionic permeability and activation of membrane-bound enzymes, as well as the classical genomic effect involving estrogen receptor activation and gene expression.

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Section: Oxidative Stress -Reactive Oxygen Speciesmentioning

confidence: 99%

Effects of estrogen on the vascular system

Tostes

Nigro

Fortes

et al. 2003

Braz J Med Biol Res

173

126

View full text Add to dashboard Cite

show abstract

“…Enhanced oxidative stress may be another factor contributing to this dysfunction, although controversy remains [66]. A recent study in normotensive women showed that endothelial dysfunction secondary to acute endogenous estrogen deprivation is strongly linked to a reduction in the bioavailability of ·NO [67]. Moreover, E 2 can attenuate O 2 −· formation in phagocytes [68] and endothelial cells [6].…”

Section: Discussionmentioning

confidence: 99%

17β-Estradiol reverses shear-stress-mediated low density lipoprotein modifications

Hwang¹,

Rouhanizadeh²,

Hamilton³

et al. 2006

Free Radical Biology and Medicine

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Within arterial bifurcations or branching points, oscillatory shear stress (OSS) induces oxidative stress mainly via the NADPH oxidase system. It is unknown whether 17β-estradiol (E 2 ) can regulate OSS-mediated low density lipoprotein (LDL) modifications. Bovine aortic endothelial cells (BAECs) were pre-treated with E 2 at 5 nmol/L, followed by exposure to OSS (0 ± 3.0 dynes/ cm 2 sec and 60 cycles/min) in a flow system. E 2 decreased OSS-mediated NADPH oxidase mRNA expression, and E 2 -mediated ·NO production was mitigated by the ·NO synthase inhibitor L-NAME. The rates of O 2 −· production in response to OSS increased steadily as determined by superoxide dismutase-inhibited ferricytochrome c reduction; however, pre-treatment with E 2 decreased OSS-mediated O 2 −· production (n=4, P<0.05). In the presence of native LDL (50 μg/ mL), E 2 also significantly reversed OSS-mediated LDL oxidation as determined by high performance liquid chromatography. In the presence of O 2 −· donor, xanthine oxidase (XO), E 2 further reversed XO-induced LDL lipid peroxidation (n=3, P<0.001). Mass spectra were acquired in the m/z 400-1800 range, revealing XO-mediated LDL protein nitration involving tyrosine 2535 in the α-2 domains, whereas pre-treatment with E 2 reversed this observation, consistent with the changes in nitrotyrosine intensities by the dot blots. E 2 plays an indirect antioxidative role. In addition to up-regulation of eNOS and down-regulation of Nox4 expression, E 2 influences LDL modifications via lipid peroxidation and protein nitration.

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“…De fato, a presença de receptores de estrogênio no coração, músculo liso vascular, no cérebro (núcleo do trato solitário e medula ventrolateral), as modificações na densidade de receptores adrenérgicos, nos níveis de AMPc e na NO sintase são sugestivas do possível envolvimento desse hormônio na regulação do sistema cardiovascular (Perrot-Applanat, 1996;Virdis et al, 2000). Estudos que demonstram diversas alterações ocorridas durante o ciclo estral normal, tais como intolerância ortostática, síncope, edema, variações de volume plasmático e alterações na regulação do sistema nervoso simpático dão suporte a essa participação (Thompson et al, 1988;De Souza et al, 1989;Hassan et al, 1990;Scott et al, 1990;Endicott J, 1993;Jacob et al, 1997;Jacob et al, 2000).…”

Section: Descritoresunclassified

“…Narkiewicz et al (2005) Além da ANSP, indivíduos com idade avançada parecem apresentar redução de fluxo sangüíneo e, portanto, aumento de resistência vascular (Moreau et al, 2002). De fato, essa variável parece estar diminuída com o envelhecimento, tanto em homens como em mulheres, sendo mediada tanto pela redução de oxido nítrico circulante quanto pelo aumento de secreção de endotelina (Dinenno et al, 1999;Virdis et al, 2000;Taddei et al, 2001). …”

Section: Envelhecimentounclassified

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Avaliação da atividade nervosa simpática periférica em mulheres jovens e em pós-menopausadas

Bernardo¹

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Mechanisms Responsible for Endothelial Dysfunction Associated With Acute Estrogen Deprivation in Normotensive Women

Abstract: Endothelial dysfunction secondary to acute endogenous estrogen deprivation is caused by reduced NO availability. Cyclooxygenase-dependent production of oxidative stress could be responsible for this alteration.

Cited by 149 publications

References 54 publications

Effects of estrogen on the vascular system

Effects of estrogen on the vascular system

17β-Estradiol reverses shear-stress-mediated low density lipoprotein modifications

Avaliação da atividade nervosa simpática periférica em mulheres jovens e em pós-menopausadas

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