The vascular alterations in diabetic male rats are well characterized. But few studies has been made in female. Women have a lower risk of developing cardiovascular disease when compared to men, a beneficial effect of estrogen on the cardiovascular system can be associated, however, in female diabetic this is lost. The main cardioprotective action of estrogen are mediated by estrogen receptor ESR1/ERa, this estrogen receptor increased the activation of the nitric oxide synthase (NOS) endothelial and also reduced the inducible NOS (iNOS) expression. On the other hand, it has been observed that estrogen receptor ESR2 activation induces expression of iNOS. The mechanism whereby female diabetic loses the protective effect of the estrogen in the cardiovascular system is still unclear, but changes in the pattern of estrogen receptor expression ESR1/ER± and ESR2/ER² may be involved. Diabetes promotes alterations in the receptor estrogen expression pattern with ESR2 increased. We previously observed reduced contractile response in aortas of diabetic female rats, but the mechanisms were not investigated. In order that, the ERS2 expression is increased in diabetic male rats aorta and that this receptor leads to iNOS increased and that high concentration of NO is cytotoxic, then the objective of this study is analyze whether ERS2 may participate in the vasoconstrictor attenuation in diabetic female rats aorta.
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