Is estradiol cardioprotection a nitric oxide-mediated effect?

Duncan, A. C.; Petrie, J. R.; Brosnan, M J; Devlin, Alison M.; Bass, Roman; Charnock‐Jones, D. Stephen; Connell, Jmc; Dominiczak, Anna F.; Lumsden, Mary-Ann

doi:10.1093/humrep/17.7.1918

Cited by 7 publications

(6 citation statements)

References 46 publications

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“…Among the hypothesis that may explain the protective effect of oestrogens (E) there are the following: E can suppress the synthesis of collagen and fibronectin, proteins that are increased in nephropathies [9]; E reduce the accumulation of LDL in coronary arteries, they can activate muscarinic receptors, thus stimulating endothelial cells to synthesize nitric oxide (NO) and, consequently, increase the circulating levels of nitrates and nitrites [10]. E reduce the entry of extracellular calcium into the vascular smooth muscle [11], decrease the affinity of receptors to vasoconstrictors and have a relaxing effect on vessels, decreasing levels of endothelin and norepinephrine [12], besides having antioxidant properties against ROS [13,14].…”

Section: Introductionmentioning

confidence: 99%

Association of renal damage and oxidative stress in a rat model of metabolic syndrome. Influence of gender

Pérez-Torres¹,

Roque²,

Hafidi

et al. 2009

Free Radical Research

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This study investigated the association between nephropathy and oxidative stress, by measurement of systolic blood pressure, lipid peroxidation, activities of catalase, manganese- and copper-zinc-superoxide dismutase and endothelial nitric oxide synthase expression and concentrations of nitrates/nitrites in kidneys from rats with Metabolic Syndrome. Weaning female or male rats had 30% sucrose to drink for 24 weeks (Metabolic Syndrome). Modulation by sex hormones was investigated by gonadectomy and hormone replacement. In Metabolic Syndrome, Castrated Metabolic Syndrome + Testosterone males and Ovariectomized Metabolic Syndrome females had increased blood pressure, proteinuria and lipid peroxidation. Nitrates/nitrites and activities of catalase, manganese and copper-zinc-superoxide dismutase decreased vs intact Control, Castrated Metabolic Syndrome males, intact Metabolic Syndrome and Ovariectomized Metabolic Syndrome + Estradiol females. The results suggest that sex hormones modulate the activity of superoxide-dismutase, catalase and endothelial nitric oxide-synthase. Ovariectomy decreased the protection against oxidative stress in females; the opposite occurred in castrated males.

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Section: Introductionmentioning

confidence: 99%

Association of renal damage and oxidative stress in a rat model of metabolic syndrome. Influence of gender

Pérez-Torres¹,

Roque²,

Hafidi

et al. 2009

Free Radical Research

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“…After treating human aortic endothelial cells with 17beta estradiol and measuring eNOS expression after 24 hour and 7 day regimens using intro-arterial infusion of interbrachial N Gmonomethyl-1-arginine, it was determined that there was no change in eNOS expression after acute or chronic estradiol treatment. A study by the same group (350) in which the vasoconstrictor response to a substrate inhibitor of nitric oxide synthase was measured in 10 healthy postmenopausal women receiving 80µg transdermal estrogen daily for four weeks also showed no difference in vasoconstrictor responses as mediated by nitric oxide.…”

Section: Estrogen and Testosteronementioning

confidence: 95%

“…Another recent study focused in on the questions as to whether estrogen's cardioprotective effect is a function of its effect on nitric oxide production (350). After treating human aortic endothelial cells with 17beta estradiol and measuring eNOS expression after 24 hour and 7 day regimens using intro-arterial infusion of interbrachial N Gmonomethyl-1-arginine, it was determined that there was no change in eNOS expression after acute or chronic estradiol treatment.…”

Section: Estrogen and Testosteronementioning

confidence: 99%

“…It has also been shown that estrogen administration may effect the vasodilator response to acetylcholine (350). There is evidence that oestrogen modulates the vasodilator response to acetylcholine in rabbit aortas, (351) and that continuous estrogen administration can reduce the acetylcholine-induced vasoconstriction in atherosclerotic ovariectomized monkeys (352).…”

Section: Estrogen and Testosteronementioning

confidence: 99%

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Intracellular signaling mechanisms of sex hormones in acute myocardial inflammation and injury

Meldrum

Wang²,

Tsai

et al. 2005

Front Biosci

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Sex hormones are important modifiers of the acute inflammatory response to injury, an important aspect of myocardial depression and apoptosis following ischemia or endotoxemia. Hemorrhage, trauma, ischemia/reperfusion, burn and sepsis each lead to cardiac dysfunction. Gender has been shown to influence the inflammatory response as well as outcomes following acute injury. The mechanisms by which sex affects the inflammatory response and the outcome to acute injury are being actively investigated. It is now recognized that myocardial inflammation plays a crucial role in I/R-induced myocardial dysfunction. Inflammatory mediators, such as TNF-alpha are produced by cardiomyocytes and contribute to myocardial functional depression and apoptosis. Gender differences in the inflammatory response following burn injury have been demonstrated. However, gender differences in the setting of acute I/R-induced inflammation are unclear. In addition, a critical component of the signal transduction pathway leading to myocardial inflammation is the activation of p38 mitogen-activated protein kinase (MAPK). In other systems, it appears that gender differences exist in the p38 MAPK signaling pathway. The inflammatory response, including the p38 MAPK signaling cascade and expression of proinflammatory cytokines such as TNF-alpha and IL-1beta, may precipitate cardiomyocyte apoptosis following I/R injury. Apoptosis may be an essential component in the pathogenesis of heart failure, and there is evidence that myocyte apoptosis in the failing human heart is markedly lower in women than in men. The prevention of cell death attenuates I/R-induced injury on myocardial anatomy and performance. This review will: 1) examine evidence for gender differences in the outcome to acute injury; 2) explain the myocardial inflammatory response to acute injury; and 3) elucidate the various mechanisms by which gender and sex hormones affect the myocardial response to acute injury.

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“…Por outro lado, a perda da proteção hormonal com a falência ovariana na produção de estrogênios na pós-menopausa leva ao aumento do risco de DCV 1 . Sabe-se que o papel preventivo dos esteroides sexuais femininos foi sugerido pela primeira vez há mais de meio século, o que foi confirmado por inúmeros estudos nos quais a terapia de reposição hormonal estaria associada com a redução das DCV em mulheres na pós-menopausa 2 . Contudo, mulheres com idade superior a 65 anos ou com mais de 10 anos de menopausa sofreriam o efeito contrário, ou seja, incremento do risco de DCV 3 .…”

Section: Introductionunclassified

Morfologia dos cardiomiócitos e quantificação do colágeno no miocárdio de ratas tratadas com isoflavonas ou estrogênios

Cabanelas¹,

Carbonel²,

Santos³

et al. 2012

Rev. Bras. Ginecol. Obstet.

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Morfologia dos cardiomiócitos e quantificação do colágeno no miocárdio de ratas tratadas com isoflavonas ou estrogênios Cardiomyocytes morphology and collagen quantification in the myocardium of female rats treated with isoflavones or estrogensResumo OBJETIVOS: Avaliar a morfologia dos cardiomiócitos e quantificar o colágeno presente no miocárdio de ratas tratadas com extrato concentrado de soja ou 17β-estradiol (E2). MÉTODOS: Vinte e oito ratas foram divididas em quatro grupos: GCtrl -fase de estro; GOvx -ovariectomizadas (Ovx); GIso -Ovx tratadas com extrato de soja (150 mg/kg, por dia); GE2 -Ovx tratadas com E2 (10 μg/kg, por dia). As drogas e o veículo (0,2 mL de propilenoglicol) foram administrados após 30 dias da realização da ovariectomia, por 30 dias consecutivos. No último dia os animais foram anestesiados, o coração retirado, mergulhado em formaldeído a 10%, e fragmentos dos ventrículos submetidos a processamento histológico, sendo os cortes corados pela hematoxilina e eosina ou pelo picrosirius-red. As análises histomorfométricas (contagem, volume nuclear e quantificação do colágeno) foram realizadas em microscópio de luz e software AxioVision Rel. 4.2, sendo o colágeno determinado pelo programa Imagelab 2000. Os dados foram submetidos ao teste de ANOVA complementado pelo teste de Tukey (p<0,05). RESULTADOS: Notamos maior quantidade de núcleos de cardiomiócitos nos animais dos grupos Ovx e Iso do que no GE2 e GCtrl (GOvx=121,7±20,2=GIso=92,8±15,4>GE2=70,5±14,8=GCtrl=66,3±9,6; p<0,05), sendo o volume nuclear maior nos animais do grupo Ctrl e E2 (GE2=35,7±4,8=GCtrl=29,9±3,6>GIso=26,5±4,5= GOvx=22,4±2,9; p<0,05). Com relação ao colágeno notamos maior concentração no grupo Ovx (GOvx=5, 4±0,1>GCtrl=4,0±0,1=GIso=4,4±0,08=GE2=4,3±0,5; p<0,05). CONCLUSÕES: Os estrogênios previnem a diminuição do volume nuclear dos cardiomiócitos e a deposição de colágeno entre as fibras musculares cardíacas. Já a administração de isoflavonas previne somente a deposição de colágeno, o que pode preservar as propriedades mecânicas das fibras cardíacas. Abstract PURPOSES:To evaluate the histomorphometry of cardiomyocytes and collagen present in the myocardium of rats treated with a concentrated extract of soy or 17β-estradiol (E2). METHODS: Twenty-eight rats were divided into four groups: GCtrl -estrus phase; GOvx -ovariectomized (Ovx) and receiving vehicle; GIso -Ovx and treated with soy extract (150 mg/kg per day); GE2 -Ovx and treated with E2 (10 μg/kg per day). The drugs and vehicle (0.2 mL propylene glycol) were administered for 30 consecutive days after ovariectomy. On the last day the animals were anesthetized, the hearts removed, submerged in 10% formaldehyde and fragments of the ventricles underwent histological procedures, and the sections were stained with hematoxylin and eosin or picrosirius-red. Histomorphometric analysis (number and volume of nuclei and quantification of collagen) was performed under a light microscope with AxioVision Rel. 4.2 software, and collagen fibers were quantified using IMAGELAB-2000 softwar...

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Is estradiol cardioprotection a nitric oxide-mediated effect?

Abstract: The present studies do not provide evidence for an eNOS-mediated cardioprotective response to estrogen and therefore suggest that additional mechanisms other than the endothelial NO system may have an important role in the cardiovascular effects of estrogen.

Cited by 7 publications

References 46 publications

Association of renal damage and oxidative stress in a rat model of metabolic syndrome. Influence of gender

Association of renal damage and oxidative stress in a rat model of metabolic syndrome. Influence of gender

Intracellular signaling mechanisms of sex hormones in acute myocardial inflammation and injury

Morfologia dos cardiomiócitos e quantificação do colágeno no miocárdio de ratas tratadas com isoflavonas ou estrogênios

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