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首页> 外文期刊>Life sciences >Bone medullary arterioles from ovariectomized rats have smaller baseline diameters but normal eNOS expression and NO-mediated dilation
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Bone medullary arterioles from ovariectomized rats have smaller baseline diameters but normal eNOS expression and NO-mediated dilation

机译：去卵巢大鼠的骨髓髓小动脉的基线直径较小，但是正常的eNOS表达和NO介导的扩张

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This study was designed to test the hypothesis that endogenous estrogens decrease the expression of endothelial nitric oxide synthase (eNOS) in resistance-size bone arterioles, thereby reducing endothelium-dependent vasodilator function. Sexually mature female rats were ovariectomized to reduce endogenous estrogens. Age-matched female rats served as controls. Seven to ten days after ovariectomy, bone marrow tissue was collected from the femoral canal. Immuno-histochemistry was performed to detect expression of estrogen receptors, alpha and beta and eNOS. eNOS protein content in medullary bone arterioles was compared using Western blot analysis. Endothelial cell function was assessed by quantitating the dilation of isolated, pressurized bone arterioles in response to acetylcholine. The results indicate that the endothelium of bone arterioles from ovariectomized and control rats express ER-alpha, ER-beta and eNOS. eNOS protein content in the two groups of arterioles did not differ. However, the baseline diameter of arterioles from ovariectomized rats (63 +/- 4 mu m) was significantly smaller than the diameter of arterioles from control rats (75 +/- 3 mu m, p < 0.05). The two groups of arterioles dilated equally in response to acetylcholine. L-NAME, an inhibitor of eNOS, almost completely abolished the dilator responses to acetylcholine, but not to sodium nitroprusside. L-Arginine restored acetylcholine-induced dilation after L-NAME treatment. Thus, arteriole dilation to acetylcholine appears to be mediated almost exclusively by NO. The smaller diameter of arterioles from ovariectomized rats suggests that endogenous estrogens exert a significant dilator influence on bone arterioles. However, the dilator influence does not appear to be mediated by an increase in eNOS expression or enhanced NO-dependent vasodilation. These results indicate that estrogens do not decrease eNOS expression or diminish NO-mediated dilation of bone medullary arterioles. (c) 2005 Published by Elsevier Inc.
机译：本研究旨在检验以下假设：内源性雌激素会降低抗性大小的骨小动脉中内皮型一氧化氮合酶（eNOS）的表达，从而降低内皮依赖性血管舒张功能。将性成熟的雌性大鼠切除卵巢以减少内源性雌激素。年龄匹配的雌性大鼠作为对照。卵巢切除术后七至十天，从股管收集骨髓组织。进行免疫组织化学以检测雌激素受体，α和β以及eNOS的表达。使用蛋白质印迹分析比较了髓质骨小动脉中的eNOS蛋白含量。通过量化对乙酰胆碱反应的分离的加压骨小动脉的扩张来评估内皮细胞功能。结果表明，去卵巢和对照大鼠的骨小动脉内皮表达ER-α，ER-β和eNOS。两组小动脉中的eNOS蛋白含量没有差异。但是，去卵巢大鼠的小动脉的基线直径（63 +/- 4微米）显着小于对照大鼠的小动脉的直径（75 +/- 3微米，p <0.05）。两组小动脉对乙酰胆碱的反应均等地扩张。 eNOS抑制剂L-NAME几乎完全消除了扩张剂对乙酰胆碱的反应，而不是对硝普钠的反应。 L-NAME治疗后，L-精氨酸恢复了乙酰胆碱诱导的扩张。因此，小动脉扩张为乙酰胆碱似乎几乎完全由NO介导。去卵巢大鼠的小动脉直径较小，表明内源性雌激素对骨小动脉具有明显的扩张作用。但是，扩张剂的影响似乎不由eNOS表达的增加或NO依赖性血管舒张增强引起。这些结果表明，雌激素不会降低eNOS表达或减少NO介导的骨髓小动脉扩张。 （c）2005年由Elsevier Inc.发布。

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