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首页> 外文期刊>American Journal of Physiology >Effect of estrogen on cerebrovascular prostaglandins is amplified in mice with dysfunctional NOS.
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Effect of estrogen on cerebrovascular prostaglandins is amplified in mice with dysfunctional NOS.

机译：在功能异常的NOS小鼠体内，雌激素对脑血管前列腺素的作用被放大。

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Chronic estrogen treatment increases endothelial vasodilator function in cerebral arteries. Endothelial nitric oxide (NO) synthase (eNOS) is a primary target of the hormone, but other endothelial factors may be modulated as well. In light of possible interactions between NO and prostaglandins, we tested the hypothesis that estrogen treatment increases prostanoid-mediated dilation using NOS-deficient female mouse models, i.e., mice treated with a NOS inhibitor [N(G)-nitro-l-arginine methyl ester (l-NAME)] for 21 days or transgenic mice with the eNOS gene disrupted (eNOS(-/-)). All mice were ovariectomized; some in each group were treated chronically with estrogen. Cerebral blood vessels then were isolated for biochemical and functional analyses. In vessels from control mice, estrogen increased protein levels of eNOS but had no significant effect on cyclooxygenase (COX)-1 protein, prostacyclin production, or constriction of pressurized, middle cerebral arteries to indomethacin, a COX inhibitor. In l-NAME-treated mice, however, cerebrovascular COX-1 levels, prostacyclin production, and constriction to indomethacin, as well as eNOS protein, were all greater in estrogen-treated animals. In vessels from eNOS(-/-) mice, estrogen treatment also increased levels of COX-1 protein and constriction to indomethacin, but no effect on prostacyclin production was detected. Thus cerebral blood vessels of control mice did not exhibit effects of estrogen on the prostacyclin pathway. However, when NO production was dysfunctional, the impact of estrogen on a COX-sensitive vasodilator was revealed. Estrogen has multiple endothelial targets; estrogen effects may be modified by interactions among these factors.
机译：慢性雌激素治疗可增加脑动脉内皮血管舒张功能。内皮型一氧化氮（NO）合酶（eNOS）是该激素的主要靶标，但其他内皮因子也可能受到调节。考虑到NO和前列腺素之间可能存在的相互作用，我们测试了以下假设：雌激素治疗可使用NOS缺陷型雌性小鼠模型（即用NOS抑制剂[N（G）-硝基-1-精氨酸甲基酯（l-NAME）] 21天或eNOS基因被破坏的转基因小鼠（eNOS（-/-））。所有小鼠均被切除卵巢。每组中的一些患者长期接受雌激素治疗。然后分离脑血管进行生化和功能分析。在对照小鼠的血管中，雌激素可增加eNOS的蛋白质水平，但对环氧合酶（COX）-1蛋白，前列环素的产生或加压中脑动脉对吲哚美辛（一种抑制COX的抑制剂）的作用无明显影响。然而，在用l-NAME治疗的小鼠中，在用雌激素治疗的动物中，脑血管COX-1的水平，前列环素的产生和吲哚美辛的收缩以及eNOS蛋白都更高。在来自eNOS（-/-）小鼠的血管中，雌激素治疗还增加了COX-1蛋白的水平并抑制了吲哚美辛，但未检测到对前列环素产生的影响。因此，对照小鼠的脑血管未表现出雌激素对前列环素途径的作用。但是，当NO产生功能障碍时，就会显示出雌激素对COX敏感的血管扩张剂的影响。雌激素具有多个内皮靶标;这些因素之间的相互作用可能会改变雌激素的作用。

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