Postmenopause, characterized by estrogen deficiency, contributes to the risk of cardiovascular dysfunction. The purpose of this study was to investigate the combined effects of chronic exercise and estrogen on vascular function in ovariectomized rats. Fifteen‐week‐old female Sprague‐Dawley rats were randomly assigned into 3 groups: sham‐operated (sham), ovariectomized (OVX), and OVX with given exercise and 17 beta‐estradiol injection (OVX+Ex+E2) groups. The thoracic aortas were dissected for acetylcholine (ACh)‐ and insulin‐like growth factor‐1 (IGF‐1)‐mediated vasodilation analysis. To explore the roles of phosphatidylinositol‐3 kinase (PI3K) and NO synthase (NOS), selective inhibitors (i.e., wortmannin and Nω‐nitro‐L‐arginine methyl ester) were used. Sodium nitroprusside (SNP, a NO donor)‐induced vasodilation was also examined. We found that, 1) compared with sham rats, the vasodilation evoked by ACh and IGF‐1 was significantly deteriorated in OVX rats, but the effects were disappeared after the removal of endothelium; 2) the combined intervention significantly improved ACh‐ and IGF‐1‐mediated vasodilation in OVX rats; 3) these altered vascular responses were mainly mediated by the release of PI3K and NOS; 4) no significant difference in SNP‐mediated vasodilation was found among three groups. According to our results, we suggested that chronic exercise and estrogen may cooperatively reverse postmenopause‐altered vascular function.
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