Although aging is known to lead to increased vascular stiffness, the role of estrogens in the prevention of age-related changes in the vasculature remains to be elucidated. To address this, we measured vascular function in the thoracic aorta in adult and old ovariectomized (ovx) rats with and without immediate 17beta-estradiol (E2) replacement. In addition, aortic mRNA and protein were analyzed for proteins known to be involved in vasorelaxation. Aging in combination with the loss of estrogens led to decreased vasorelaxation in response to acetylcholine and sodium nitroprusside, indicating either smooth muscle dysfunction and/or increased fibrosis. Loss of estrogens led to increased vascular tension in response to phenylephrine, which could be partially restored by E2 replacement. Levels of endothelial nitric oxide synthase and inducible nitric oxide synthase did not differ among the groups, nor did total nitrite plus nitrate levels. Old ovx exhibited decreased expression of both the alpha and beta-subunits of soluble guanylyl cyclase (sGC) and had impaired nitric oxide signaling in the vascular smooth muscle. Immediate E2 replacement in the aged ovx prevented both the impairment in vasorelaxation, and the decreased sGC receptor expression and abnormal sGC signaling within the vascular smooth muscle.

译文

尽管已知衰老会导致血管僵硬,但仍需阐明雌激素在预防与年龄相关的脉管系统变化中的作用。为了解决这个问题,我们在有和没有立即进行17beta-雌二醇(E2)替代的成年和卵巢切除的成年(ovx)大鼠中测量了胸主动脉的血管功能。另外,分析了主动脉mRNA和蛋白质中已知与血管舒张有关的蛋白质。衰老与雌激素的丧失相结合导致对乙酰胆碱和硝普钠的反应引起的血管舒张减少,表明平滑肌功能障碍和/或纤维化增加。雌激素的丢失导致对苯肾上腺素的反应,血管紧张性增加,这可以通过E2替代而部分恢复。两组间内皮型一氧化氮合酶和可诱导型一氧化氮合酶的水平无差异,总亚硝酸盐和硝酸盐的水平也无差异。老ovx表现出可溶性鸟苷酰环化酶(sGC)的α和β亚基的表达减少,并且血管平滑肌中的一氧化氮信号传导受损。立即在老年ovx中进行E2置换可预防血管舒张受损,血管平滑肌内sGC受体表达降低和sGC信号异常。

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