Department of Comparative Biomedical Sciences, Louisiana State University School of Veterinary Medicine, Baton Rouge, USA.
Antioxid Redox Signal. 2012 Jan 15;16(2):139-52. doi: 10.1089/ars.2011.3967. Epub 2011 Sep 22.
Exercise training (ExT) is a recommended adjunct to many pharmaceutical antihypertensive therapies. The effects of chronic ExT on the development of hypertension-induced renal injury remain unknown. We examined whether ExT would preserve renal hemodynamics and structure in the spontaneously hypertensive rat (SHR), and whether these effects were mediated by improved redox status and decreased inflammation. Normotensive WKY rats and SHR underwent moderate-intensity ExT for 16 weeks. One group of SHR animals was treated with hydralazine to investigate the pressure-dependent/independent effects of ExT. Acute renal clearance experiments were performed prior to sacrifice. Tissue free radical production rates were measured by electron paramagnetic resonance; gene and protein expression were measured by real time RT-PCR and Western blot or immunofluorescence, respectively. Plasma angiotensin II levels and kidney antioxidants were assessed. Training efficacy was assessed by citrate synthase activity assay in hind-limb muscle.
ExT delayed hypertension, prevented oxidative stress and inflammation, preserved antioxidant status, prevented an increase in circulating AngII levels, and preserved renal hemodynamics and structure in SHR. In addition, exercise-induced effects, at least, in part, were found to be pressure-independent.
This study is the first to provide mechanistic evidence for the renoprotective benefits of ExT in a model of hypertension. Our results demonstrate that initiation of ExT in susceptible patients can delay the development of hypertension and provide renoprotection at the functional and ultrastructural level.
Chronic ExT preserves renal hemodynamics and structure in SHR; these effects are partially mediated by improved redox status and decreased inflammation.
运动训练（ExT）是许多抗高血压药物治疗的推荐辅助手段。慢性 ExT 对高血压引起的肾损伤发展的影响尚不清楚。我们研究了 ExT 是否会保留自发性高血压大鼠（SHR）的肾脏血液动力学和结构，以及这些作用是否通过改善氧化还原状态和减少炎症来介导。正常血压的 WKY 大鼠和 SHR 接受了 16 周的中等强度的 ExT。一组 SHR 动物接受肼屈嗪治疗，以研究 ExT 的压力依赖/独立效应。在牺牲前进行急性肾清除实验。通过电子顺磁共振测量组织自由基产生率；通过实时 RT-PCR 和 Western blot 或免疫荧光分别测量基因和蛋白质表达。评估血浆血管紧张素 II 水平和肾脏抗氧化剂。通过后肢肌肉中的柠檬酸合酶活性测定评估训练效果。
ExT 延迟了高血压的发生，预防了氧化应激和炎症，维持了抗氧化状态，防止了循环 AngII 水平的升高，并保留了 SHR 的肾脏血液动力学和结构。此外，运动引起的效应至少部分是压力独立的。
这项研究首次为 ExT 在高血压模型中的肾脏保护作用提供了机制证据。我们的结果表明，在易感患者中开始 ExT 可以延迟高血压的发展，并在功能和超微结构水平上提供肾脏保护。
慢性 ExT 保留了 SHR 的肾脏血液动力学和结构；这些作用部分通过改善氧化还原状态和减少炎症来介导。
