Effects of estrogen on the vascular system

Tostes, Rita C.; Nigro, Dorothy; Fortes, Zuleica Bruno; Carvalho, Marina Vieira de

doi:10.1590/s0100-879x2003000900002

Cited by 167 publications

(144 citation statements)

References 63 publications

(56 reference statements)

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“…Although prior studies showed that iNOS transfection reduces neointimal growth (15), the simultaneous increases in iNOS message, lumen loss and collagen accumulation observed in the present study raise the hypothesis that iNOS activity may be involved in constrictive vascular remodeling. In agreement with our findings, in the unilateral carotidtying model, iNOS knock-out mice showed reduced constrictive remodeling without a change in neointima, which was decreased only in the eNOS knock-out mice (17).…”

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confidence: 86%

Estrogen enhances vasoconstrictive remodeling after injury in male rabbits

Francisco

Dantas

Carvalho

et al. 2005

Braz J Med Biol Res

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The complete spectrum of estrogen vascular effects remains unclear. In particular, estrogen effects in the vascular response to profound injury in males have not been explored in detail. Therefore, we submitted 44 male New Zealand rabbits weighing 3.4 ± 0.6 kg to overdistention balloon injury of the right iliac artery. Rabbits were given 17ß-estradiol (5.45 µmol/day, sc) or vehicle for 7 days before and 14 days after injury, when the arteries were examined by postmortem histomorphometry. Arteriographic caliber was assessed in vivo at baseline and before sacrifice. On day 14 after injury, in vivo arteriographic caliber (baseline = 2.44 ± 0.43 mm) was decreased by 23.1 ± 0.1% in controls and by 44.5 ± 0.1% in estrogen-treated rabbits (P < 0.001). Neither the neointimal area nor the neointima/media area ratio changed after estrogen treatment. Collagen fraction was increased in the media and neointima of estrogen-treated rabbits vs control (1.38 ± 1.30 vs 0.35 ± 0.67, respectively, P = 0.01). Taken together, these findings suggest that estrogen increased negative vascular remodeling. Transcription of endothelial and inducible nitric oxide synthases (eNOS and iNOS) was analyzed by RT-PCR. eNOS mRNA expression was marginally increased after estrogen (P = 0.07) and injury. iNOS mRNA was increased 2-to 3-fold on day 14 after injury. With estrogen treatment, iNOS mRNA increased in uninjured arteries and exhibited a further 5.5-fold increase after injury. We concluded that estrogen increased lumen loss after balloon injury in male rabbits, likely by increased negative remodeling, which may be related to increased iNOS transcriptional rates.

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confidence: 86%

Estrogen enhances vasoconstrictive remodeling after injury in male rabbits

Francisco

Dantas

Carvalho

et al. 2005

Braz J Med Biol Res

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“…There are a number of different mechanisms proposed by which estrogen may bring about its beneficial effects on the cardiovascular system. In humans and experimental animals, estrogen facilitates vasodilation by stimulating prostacyclin and nitric oxide synthesis as well as by decreasing the production of vasoconstrictor substances, such as cyclooxygenase-derived products, reactive oxygen species, angiotensin II, and endothelin-1 (3). Estrogen also reduces the number of adrenal angiotensin type I (AT 1 ) receptors, but indirectly, by modulating adrenal angiotensin II (4).…”

Section: T Here Has Been Much Interest In the Cardiovascularmentioning

confidence: 99%

Aromatase-Deficient (ArKO) Mice Have Reduced Blood Pressure and Baroreflex Sensitivity

Head

Obeyesekere

Jones³

et al. 2004

Endocrinology

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Aromatase-deficient (ArKO) mice are deficient in estrogens due to deletion of the aromatase gene. We hypothesized that there may be changes in the cardiovascular system of ArKO mice because of evidence linking estrogens with improved cardiovascular outcomes and the induction of the glucocorticoid-metabolizing enzyme, 11␤-hydroxysteroid dehydrogenase type 2 (11␤HSD2), gene in the kidney, which is important for the regulation of blood pressure (BP). BP and baroreflex sensitivity (BRS) in female conscious ArKO mice were compared with those in age-and weight-matched wild-type (WT) mice. Power spectral analysis was used to determine cardiovascular variability and BRS. Although systolic BP was similar in the two groups, diastolic and mean BPs were lower in the ArKO mice (؊6.3 ؎ 1.9 and ؊4.6 ؎ 2.1 mm Hg, respectively).Heart rate (HR) was greater in the ArKO mice (؉36 ؎ 6 beats/ min). The mean BP in WT mice was 105 mm Hg, and the HR was 481 beats/min. In the autonomic frequency range, BP variability was 74% greater, and HR variability was only 26% that in WT mice. The BRS of ArKO mice was 46% of the value observed in WT mice. 11␤HSD2 levels were unaltered in ArKO mice, except in the kidney, where they were only 10% of WT levels. Estradiol administration to ArKO mice restored renal 11␤HSD2 to WT levels. The results show that ArKO mice have lower diastolic BP, but increased BP variability, perhaps due to an impaired BRS. Thus, aromatase activity is critical for normal autonomic control of the heart and, hence, for reducing the deleterious effects of high BP variability. (Endocrinology 145: 4286 -4291, 2004)

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“…Vários outros estudos têm demonstrado efeitos diretos e diferenciados dos hormônios sexuais endógenos e exógenos no sistema cardiovascular (29)(30)(31) . O estrogênio, por exemplo, está diretamente associado a efeito cardioprotetor, pela redução da resistência local e perifé-rica, pela modulação da hipertrofia de cardiomiócitos e de células de músculo liso vascular (CMLV), através do sistema renina-angiotensina cardíaco; ou ainda estimulando a formação de fatores vasodilatadores derivados do endotélio, como óxido nítrico e prostaciclinas.…”

Section: Discussionunclassified

Uso crônico de decanoato de nandrolona como fator de risco para hipertensão arterial pulmonar em ratos Wistar

Graceli

Gava

Gomes

et al. 2010

Rev Bras Med Esporte

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RESUMOIntrodução: O uso indiscriminado de esteróides anabolizantes sintéticos, análogos à testosterona, implica aumento do risco cardiovascular e hipertrofia cardíaca. Assim, o aumento da massa ventricular direita corrigido pelo peso corporal (i.é., hipertrofia ventricular direita -HVD), poderia elevar o risco para o desenvolvimento de hipertensão arterial pulmonar (HAP). Objetivos: Examinar os efeitos do tratamento em longo prazo com decanoato de nadrolona na HVD e sua relação com a HAP em ratos. Métodos: 16 ratos Wistar com três meses de idade foram aleatoriamente divididos em dois grupos: 1) controle-sham (CONT, n = 8); 2) tratados com decanoato de nandrolona (DECA, n = 8). O tratamento consistiu na aplicação intramuscular de Deca-durabolin ® 6.0mg.kg -1 de peso corporal durante quatro semanas. Após tratamento, os animais foram anestesiados com hidrato de cloral (4.0mL.kg -1 , i.p.), submetidos à cateterização da artéria femoral para registro da pressão arterial media (PAM) e frequência cardíaca (FC). O coração, os rins e o fígado foram retirados, pesados e avaliados os índices de hipertrofia, os quais foram calculados pela razão da massa do órgão pelo peso corporal (mg.g -1 ). Resultados: Os animais tratados com DECA apresentaram aumento (p < 0,01) do peso corporal (338 ± 6g) vs. CONT (315 ± 5g). Não houve alterações da PAM, embora houvesse (p < 0,01) bradicardia nos animais tratados com DECA (321 ± 13bpm) vs. CONT (368 ± 11bpm). Verificou-se significativa (p < 0,01) hipertrofia dos ventrículos e rins, mas não no fígado. A correlação entre a HVD e PAM no grupo DECA apresentou coeficiente de Pearson positivo e maior (r 2 = 0,4013) quando comparado com o controle (r 2 = 0,0003). Conclusões: Esses dados demonstram que o uso em longo prazo de decanoato de nandrolona induz importante bradicardia e HVD, o que sugere aumento do risco para HAP.Palavras-chave: esteróide anabolizante, pressão sanguínea, hipertrofia ventricular, hipertensão arterial pulmonar. ABSTRACTIntroduction: The unsystematic use of anabolic steroids, synthetic analogs of testosterone, implies enhanced cardiovascular risk and cardiac hypertrophy. Thus, increased right ventricular mass corrected by the body weight (e.g.right ventricular hypertrophy -RVH) could raise the risk for development of pulmonary arterial hypertension (PAH). Objectives: to examine the effects of long-term chronic treatment with nandrolone decanoate on the RVH and its relationship with PAH in rats. Methods: 16 three-month Wistar male rats were treated with nandrolone decanoate (6.0 mg/kg -1 body weight; DECA, n=8) or control vehicle (CONT, n=8). The drug and vehicle were administered by a single injection in the femoral muscle once a week for 4 weeks. After the treatment, rats were anesthetized with chloral hydrate (4.0mL/kg

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Effects of estrogen on the vascular system

Cited by 167 publications

References 63 publications

Estrogen enhances vasoconstrictive remodeling after injury in male rabbits

Estrogen enhances vasoconstrictive remodeling after injury in male rabbits

Aromatase-Deficient (ArKO) Mice Have Reduced Blood Pressure and Baroreflex Sensitivity

Uso crônico de decanoato de nandrolona como fator de risco para hipertensão arterial pulmonar em ratos Wistar

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