抄録
Estrogen deficiency in the menopause is associated with an increased cardiovascular risk. Endogenous estrogen has been suggested to exert vasoprotective effects through decreasing vascular oxidative stress. To investigate the mechanism of the decreasing in oxidative stress by estrogen, we examined superoxide production and antioxidant enzyme expression in aorta in ovariectomized Dahl salt-sensitive (DS) rats. Female DS rats (8 weeks old) were ovariectomized (OVX group) or sham-operated (sham group). Estrogen pellets were subcutaneously implanted in ovariectomized rats for estrogen treatment (OVX + E group). After 4 weeks of salt-loading (8% NaCl diet), blood pressure was increased in OVX group compared with sham and OVX + E groups. Superoxide production in aortic ring was higher in OVX group than in sham and OVX + E groups. Increase in superoxide production was abolished by pretreatment with diphenyleneiodonium, a NADPH oxidase inhibitor. Expression of mRNA of p22phox, a NADPH oxidase subunit, increased in aorta from OVX group compared with sham group. In contrast to p22phox, mRNA expressions of antioxidant enzymes extracellular superoxide dismutase (ecSOD) and glutathione peroxidase (GPX) were decreased in OVX rats. Expression levels of p22phox, ecSOD and GPX in OVX + E rats were not different from that in sham group. These data suggest that estrogen deficiency in ovariectomized DS rats enhances oxidative stress through increased NADPH oxidase expression and decreased antioxidant enzymes, and promotes vascular injury by salt-loading. [J Physiol Sci. 2006;56 Suppl:S74]
