RESUMO
Using organ culture of carotid artery segments from sexually mature male and female rats, we examined the effect of estradiol 17 beta on proliferation. The index of cell proliferation was [3H]thymidine uptake. Estradiol 17 beta (0.18-0.36 microM) inhibited the uptake of thymidine in a concentration-dependent manner (p < 0.05). Estradiol 17 beta inhibited [3H]thymidine uptake only in the absence of the weak estrogen receptor agonist phenol red and in carotid artery segments from sexually mature female (p < 0.01) but not male rats. Tamoxifen (0.1 and 1 microM), a partial agonist of estrogen receptors, significantly inhibited thymidine uptake (p < 0.01). However, preincubation of the segments with tamoxifen (0.1 and 1.0 microM) for 4 h before the exposure to estradiol, blocked estradiol 17 beta-induced inhibition of thymidine uptake (p < 0.05 and p < 0.01 for 0.1 and 1.0 microM, respectively). The cyclooxygenase inhibitor indomethacin (5 microM) did not affect either the basal [3H]thymidine uptake or the estradiol 17 beta-induced inhibition of that uptake. This latter finding suggests that prostacyclin or prostaglandin E2 does not mediate the inhibitory response to estradiol 17 beta. The results of these experiments suggest that estradiol 17 beta-induced inhibition of proliferation of rat carotid artery segments is mediated through activation of estrogen receptors.
Assuntos
Divisão Celular/efeitos dos fármacos , Estradiol/farmacologia , Músculo Liso Vascular/efeitos dos fármacos , Tamoxifeno/farmacologia , Animais , Artérias Carótidas/efeitos dos fármacos , Feminino , Técnicas In Vitro , Indometacina/farmacologia , Masculino , Músculo Liso Vascular/citologia , Fenolsulfonaftaleína/farmacologia , Ratos , Ratos Sprague-Dawley , Receptores de Estrogênio/efeitos dos fármacos , Fatores Sexuais , Timidina/metabolismo , Fatores de TempoRESUMO
OBJECTIVE: To determine the pathogenesis of muscular symptomatology in the eosinophilia-myalgia syndrome (EMS). METHODS: P31-nuclear magnetic resonance spectroscopy (MRS) was performed on 7 patients with EMS and 10 age matched controls to determine the relative concentrations of phosphocreatine (PCr), inorganic phosphate (Pi), and adenosine triphosphate (ATP) in calf muscle. RESULTS: Patients with EMS had statistically lower ATP/PCr ratios and higher Pi/ATP ratios than controls, indicating a preferential and unique decrease in ATP levels at rest in skeletal muscle. CONCLUSION: Skeletal muscle is metabolically abnormal in patients with EMS. This abnormality may contribute to the myalgia, spasm, and weakness seen in this disorder.
