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Effects if Estrogen on the Expression of Artery Estrogen Receptor and the Activity of Vascular Endothelial Nitric Oxide Synthase

Author: RuanYunJun
Tutor: WuSaiZhu
School: First Military Medical University
Course: Within the science of cardiovascular disease
Keywords: Estrogen Estradiol Receptor estrogen Hormone replacement therapy Nitric oxide Nitric oxide synthase Vascular endothelial cells Atherosclerosis
CLC: R540.2
Type: Master's thesis
Year: 2000
Downloads: 129
Quote: 0
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Abstract


Epidemiological studies have shown that 30-50% lower mortality than those who did not receiving estrogen replacement therapy in postmenopausal women with cardiovascular disease. Promotion of estrogen replacement therapy of estrogen on the cardiovascular protective effects of specific mechanism is not yet completely clear, still subject to certain restrictions. The benefits of estrogen on lipid metabolism and its effect on the inhibition of plaque formation can only partly explain the cardiovascular protective effects of estrogen. Has confirmed that the estrogen receptor in the vascular wall and atherosclerotic plaques than normal number of reduced or absent estrogen receptor, suggesting that estrogen receptor in estrogen cardiovascular protection mechanisms play an important role, but the arteries estrogen receptors as well as hormone replacement therapy in postmenopausal how changes, as well as the significance of this change is not yet clear; nitric oxide (NO), an endothelium-derived vascular relaxing factor, NO has anti-atherosclerosis effect reported in the literature of female rabbits artery ring NO release than the male rabbits and ovariectomized female rabbit polyclonal anti-atherosclerotic effect, suggesting that sex hormones may affect vascular NOS activity. In view of the above, this study intends to investigate the cardiovascular protective effects of estrogen from estrogen receptors and nitric oxide synthase two angles observed in ovariectomized and hormone replacement therapy on arterial estrogen receptor expression, and observed in which the role of the estrogen on cultured vascular endothelial cell NOS activity and NO release as well as estrogen receptor. : 1.50 adult female rats were randomly divided equally into four groups: group A: sham group; B group: simple ovariectomized group; the ovariectomized estrogen replacement therapy group C group: Group D: Ovariectomized pregnant Hormone replacement therapy group. Each group rats were given a normal diet, the rats were killed after two months, with put free assay plasma estrogen and progesterone concentrations; estrogen receptor radioligand binding assay artery. 2. With the pulmonary vascular endothelial cells attached method with and without phenol red 1640 medium model, observed a certain concentration of 17β-E 2 (with or without progestin, L-arginine, L - nitro-arginine, the estrogen receptor antagonist tamoxifen) the role of a certain time under vascular endothelial cNOS activity and NO production. cNOS activity enzymatic detection of hemoglobin, NO production of the Griess assay, the radioligand binding assay of vascular endothelium of the estrogen receptor. Results: 1. The radioligand binding stars Kirin method was detected in the rat carotid artery and the vascular endothelium to the estrogen receptor; 2. Group B artery estrogen receptor content was significantly lower than that in group A (P <0 knife 5); 3. Group C and Group D artery estrogen receptor content was significantly higher than that in group B (P <005); artery in Group C and Group D of estrogen receptor content was no significant difference (P> 0 knife 5); each no significant difference in group KD values; 4. Certain concentration of 17 p-E. The role 8 on four hours of vascular endothelial cell NO production significantly increased force door nmol the few IO nmol few people with control compared to P 0.05), a significant increase (P <005) and a significant reduction (P <0 knife 1); 6. Estrogen receptor antagonist tamoxifen can significantly inhibit these effects of estrogen. Conclusion: 1. The presence of estrogen receptors in the adult female rat arteries; 2. After ovariectomy decrease in the number of estrogen receptors in rat arteries: 3. Estrogen replacement therapy to maintain the artery in the amount of estrogen receptors in ovariectomized level before; 4. With the amount of progesterone in estrogen replacement therapy does not reduce the expression of estrogen receptors in the arteries; 5.17p-E. Can increase vascular endothelial NOS activity and the production of L-tons-NO; This effect is mediated by the estrogen receptor in vascular endothelial Plus progestin does not affect the role.

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