Muscle reflex in heart failure : role for angiotensin II and oxidative stress

本研究旨在验证如下假设：心血管疾病（包括心力衰竭）患者肾素-血管紧张素系统活性升高可诱导骨骼肌氧化应激，从而放大肌肉反射。大鼠植入含有血管紧张素II（AngII）的渗透泵14天。血管造影处理大鼠的肌肉反射反应（肾交感神经活动和后肢骨骼肌收缩的压力反应）明显大于假对照组。Tempol，一种超氧化物歧化酶模拟物，降低了AngII大鼠的肌肉反射反应，但在假大鼠中没有。在AngII大鼠的骨骼肌中，观察到超氧化物增加和NADPH氧化酶亚基gp91phox上调。这些结果完全支持我们的假设。

The present study was conducted to test the hypothesis that increased renin-angiotensin system activity in cardiovascular disease including heart failure induces oxidative stress in skeletal muscle, thereby exaggerating the muscle reflex. Rats were implanted with an osmotic-pump containing angiotensin II(AngII) for14days. In the AngII-treated rats, the muscle reflex responses(renal sympathetic nerve activity and pressor responses to hindlimb skeletal muscle contraction) were significantly larger than those in the sham-control rats. Tempol, a superoxide dismutase mimetic, reduced the muscle reflex responses in the AngII rats, but not in the sham rats. In skeletal muscle of the AngII rats, increased superoxide and upregulated gp91phox, a NADPH oxidase subunit, were observed. These results in total support our hypothesis.