Sex hormone modulation of serotonin-induced coronary vasodilation in isolated heart

Moysés, Margareth Ribeiro; Barker, Louis A.; Cabral, Antônio M.

doi:10.1590/s0100-879x2001000700014

Cited by 20 publications

(24 citation statements)

References 37 publications

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“…These results suggest that after treatment with deoxycholic acid the ability of coronary endothelial cells to produce relaxing factors is reduced, whereas the ability of vascular smooth muscle to respond to sodium nitrite remains unchanged. The concentration of deoxycholic acid used here is suitable for the removal of endothelial cells, as shown in a previous study by our group (20).…”

Section: Resultsmentioning

confidence: 63%

“…We found that basal CPP was significantly higher in hearts from control female rats than in those from control male rats. This sex difference in basal CPP seems to be related to the presence of ovarian sex hormones (20). With respect to the high level of CPP observed in the female group, it is known that estrogen may have indirect effects on the cardiovascular system, e.g., through an interaction with the renin-angiotensin system.…”

Section: Discussionmentioning

confidence: 94%

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Endothelial mediators of 17ß-estradiol-induced coronary vasodilation in the isolated rat heart

Santos

Abreu

Bissoli

et al. 2004

Braz J Med Biol Res

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The present study was designed to determine relaxation in response to 17ß-estradiol by isolated perfused hearts from intact normotensive male and female rats as well as the contribution of endothelium and its relaxing factors to this action. Baseline coronary perfusion pressure was determined and the vasoactive effects of 17ß-estradiol (10 µM) were assessed by in bolus administration before and after endothelium denudation by infusion of 0.25 µM sodium deoxycholate or perfusion with 100 µM L-NAME, 2.8 µM indomethacin, 0.75 µM clotrimazole, 100 µM L-NAME plus 2.8 µM indomethacin, and 100 µM L-NAME plus 0.75 µM clotrimazole. Baseline coronary perfusion pressure differed significantly between males (84 ± 2 mmHg, N = 61) and females (102 ± 2 mmHg, N = 61). Bolus injection of 10 µM 17ß-estradiol elicited a transient relaxing response in all groups, which was greater in coronary beds from females. For both sexes, the relaxing response to 17ß-estradiol was at least in part endothelium-dependent. In the presence of the nitric oxide synthase inhibitor L-NAME, the relaxing response to 17ß-estradiol was reduced only in females. Nevertheless, in the presence of indomethacin, a cyclooxygenase inhibitor, or clotrimazole, a cytochrome P450 inhibitor, the 17ß-estradiol response was significantly reduced in both groups. In addition, combined treatment with L-NAME plus indomethacin or L-NAME plus clotrimazole also reduced the 17ß-estradiol response in both groups. These results indicate the importance of prostacyclin and endothelium-derived hyperpolarizing factor in the relaxing response to 17ß-estradiol. 17ß-estradiol-induced relaxation may play an important role in the regulation of coronary tone and this may be one of the reasons why estrogen replacement therapy reduces the risk of coronary heart disease in postmenopausal women.

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Section: Resultsmentioning

confidence: 63%

Section: Discussionmentioning

confidence: 94%

Endothelial mediators of 17ß-estradiol-induced coronary vasodilation in the isolated rat heart

Santos

Abreu

Bissoli

et al. 2004

Braz J Med Biol Res

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“…Another finding is that the OVX group had a lower basal pressure than the other groups. Previous studies have demonstrated that castration reduces CPP (30,31), indicating that there are direct actions of estrogen on coronary vascular tonus, such as a cardioprotective effect. Additionally, tamoxifen therapy was able to promote a significant elevation in CPP, demonstrating that SERMs may mimic the beneficial effects of estrogen HRT.…”

Section: Discussionmentioning

confidence: 97%

Effect of tamoxifen on the coronary vascular reactivity of spontaneously hypertensive female rats

Borgo

Lopes

Gouvêa

et al. 2011

Braz J Med Biol Res

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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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Sex hormone modulation of serotonin-induced coronary vasodilation in isolated heart

Cited by 20 publications

References 37 publications

Endothelial mediators of 17ß-estradiol-induced coronary vasodilation in the isolated rat heart

Endothelial mediators of 17ß-estradiol-induced coronary vasodilation in the isolated rat heart

Effect of tamoxifen on the coronary vascular reactivity of spontaneously hypertensive female rats

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

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