Attenuation of homocysteine-induced endothelial dysfunction by exercise training.
Attenuation of homocysteine-induced endothelial dysfunction by exercise training.
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DOI：
10.1016/s0928-4680(03)00023-3
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发表时间：
2003-09-01
期刊：
影响因子：
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通讯作者：
Westerlind, Kim C.
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文献类型：
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作者：
Hayward, Reid;Ruangthai, Ratree;Westerlind, Kim C.
高同型半胱氨酸血症是心血管疾病发生的独立危险因素。内皮细胞暴露于高水平的同型半胱氨酸 (HCY) 会导致一氧化氮 (NO) 的可用性降低和血管功能受损，这两者都是动脉粥样硬化形成的早期事件。运动训练通过增加内皮一氧化氮的产生来改善血管功能，继发于负责其合成的酶——内皮一氧化氮合酶（eNOS）的增加。我们假设运动训练会增加内皮 NO 的产生，从而减轻与 HCY 暴露相关的内皮功能障碍。大鼠被随机分配到久坐组（SED）或运动组（EX）。锻炼方案包括在跑步机上跑步，速度为 20-25 m/min，坡度为 15%，每天 30 分钟，每周 5 天，持续 6 周。从 SED 和 EX 训练的大鼠获得的主动脉环与 2 mM HCY 一起孵育 120 分钟，然后暴露于去甲肾上腺素 (NE 100 nM) 以诱导血管收缩。一旦达到稳定的收缩平台，将环暴露于浓度不断增加的受体介导的内皮依赖性血管舒张剂乙酰胆碱（ACh；0.1、1、10、100 nM）。使用非受体介导的内皮依赖性血管舒张剂 A-23187 (0.1, 1, 10, 100 nM) 和内皮非依赖性血管舒张剂 NaNO(2) (0.1, 1, 10, 100 muM) 重复该过程。此外，还测定了eNOS蛋白含量和eNOS酶活性。从经过运动训练的大鼠身上获得的主动脉环表现出显着的（P
Hyperhomocysteinemia is an independent risk factor for the development of cardiovascular disease. Exposure of endothelial cells to elevated levels of homocysteine (HCY) results in decreased availability of nitric oxide (NO) and impaired vascular function, both of which are early events in atherogenesis. Exercise training improves vascular function by increasing endothelial NO production secondary to an increase in the enzyme responsible for its synthesis, endothelial nitric oxide synthase (eNOS). We hypothesized that exercise training would increase endothelial NO production, which would attenuate the endothelial dysfunction associated with HCY exposure. Rats were randomly assigned to either sedentary (SED) or exercise (EX) groups. The exercise regimen consisted of treadmill running at 20-25 m/min, 15% grade, 30 min/day, 5 day/week for 6 weeks. Aortic rings obtained from SED and EX trained rats were incubated with 2 mM HCY for 120 min, then exposed to norepinephrine (NE 100 nM) to induce vasoconstriction. Once a stable contraction plateau was achieved, rings were exposed to increasing concentrations of the receptor-mediated endothelium-dependent vasodilator acetylcholine (ACh; 0.1, 1, 10, 100 nM). This procedure was repeated with the non-receptor-mediated endothelium-dependent vasodilator A-23187 (0.1, 1, 10, 100 nM), and the endothelium-independent vasodilator, NaNO(2) (0.1, 1, 10, 100 muM). In addition, eNOS protein content and eNOS enzyme activity were determined. Aortic rings obtained from exercise trained rats demonstrated significantly (P