RESUMO
The influence of the phytoestrogen, isoflavones, on vasodilating responses of the thoracic aorta precontracted with norepinephrine, together with the stimulatory effect on uterine weight (uterotrophic effect), was investigated in ovariectomized rats. In comparison with intact rats, acetylcholine (ACh)-induced vasodilation showed a tendency to be decreased by ovariectomy. On the other hand, isoprenaline (ISO)-induced vasodilation was significantly increased by ovariectomy. Estrogen replacement (17beta-estradiol dipropionate, 300 microg/kg per week, for 1 month) completely restored the impaired ACh- and ISO-induced vasodilation caused by ovariectomy. Dietary isoflavone aglycones (containing 52% genistein, 42% daidzein and 6% glycitein) of 157 mg/kg per day (not 67 mg/kg per day) for 1 month, in addition to the effects of estrogen replacement, completely restored the impaired vasodilation caused by ovariectomy. However, the uterotrophic effect of dietary isoflavones of 157 mg/kg per day was incomplete as compared with that by estrogen replacement. These results indicate that phytoestrogen, isoflavones, certainly possess estrogenic actions on the vasodilating responses caused by ACh and ISO, as well as a weaker uterotrophic effect.
Assuntos
Acetilcolina/farmacologia , Aorta/efeitos dos fármacos , Estrogênios não Esteroides/farmacologia , Isoproterenol/farmacologia , Vasodilatação/efeitos dos fármacos , Vasodilatadores/farmacologia , Animais , Aorta/fisiologia , Dieta , Relação Dose-Resposta a Droga , Estradiol/farmacologia , Terapia de Reposição de Estrogênios , Feminino , Técnicas In Vitro , Isoflavonas/farmacologia , Modelos Animais , Ovariectomia , Fitoestrógenos , Preparações de Plantas , Ratos , Ratos WistarRESUMO
Caveolin-1 is a major component of caveolae. Recent studies have suggested a possible role of caveolin-1 in cell transformation and normal cell proliferation. To observe the behavior of caveolin-1 in living mitotic cells, we prepared cDNA constructs encoding the chimeric protein of alpha- or beta-caveolin-1 and green fluorescent protein (GFP) and transfected culture cells with them. Correct targeting of the chimera to the caveolae was confirmed by colocalization with the caveolar inositol 1,4,5-trisphosphate receptor-like protein. By time-lapse observation of mitotic MDCKII cells, the GFP-caveolin-1 chimeras were seen throughout the plasma membrane before cell division, but became markedly concentrated at the cleavage furrow during cytokinesis. Accumulation around the spindle poles was also observed at late telophase. The result showed that caveolin-1 undergoes a drastic distributional change during cell division and suggested that the protein may be involved in the cytokinetic process.
Assuntos
Caveolinas , Divisão Celular/fisiologia , Membrana Celular/metabolismo , Proteínas de Membrana/metabolismo , Animais , Sequência de Bases , Células COS , Caveolina 1 , Linhagem Celular , Primers do DNA/genética , DNA Complementar/genética , Cães , Proteínas de Fluorescência Verde , Humanos , Cinética , Proteínas Luminescentes/genética , Proteínas Luminescentes/metabolismo , Proteínas de Membrana/genética , Proteínas Recombinantes de Fusão/genética , Proteínas Recombinantes de Fusão/metabolismo , Fuso Acromático/metabolismo , TransfecçãoRESUMO
Female Wistar rats were treated with 17beta-estradiol (E2) (10 microg, s.c.) or with sesame oil for 3 days. The relaxation induced by isoproterenol (10(-9)-3 x 10(-6) M) in aortae precontracted with norepinephrine was significantly suppressed in aortae from E2-treated rats compared with the relaxation in those from control rats. N(G)-Nitro-L-arginine, a nitric oxide synthase inhibitor, inhibited isoproterenol-induced relaxation in aortae from both E2-treated and control rats. Metyrapone, a cytochrome P-450 monooxygenase inhibitor, inhibited it in aortae from control rats, but metyrapone enhanced the maximum relaxation in aortae from E2-treated rats. These results suggest that E2 modulates isoproterenol-induced vasodilation through nitric oxide and cytochrome P-450-dependent metabolites.