Hypertension in metabolic syndrome : Mechanism involved in activation of the sympathetic nervous system and therapeutic approach

在目前的研究中，我们发现大脑中氧化应激的增加，特别是在脑干的心血管中心，增强了交感神经的活性，从而导致代谢综合征中的高血压。作为活性氧产生的主要来源，我们发现血管紧张素1型受体及其相关信号通路的激活在脑内氧化应激增加中起着重要作用。此外，我们还发现代谢综合征患者存在交感神经系统激活和内皮功能障碍。血管紧张素受体阻滞剂的治疗改善了这些异常。

In the present study, we found that the increased oxidative stress in the brain, particularly in the cardiovascular center in the brainstem, enhanced sympathetic activity thereby causing hypertension in metabolic syndrome. As a major source of reactive oxygen species generation, we found that activation of the angiotensin type 1 receptors and related signaling pathway play an important role in the increased oxidative stress in the brain. In addition, we found that activation of the sympathetic nervous system and endothelial dysfunction occurred in patients with metabolic syndrome. Treatment with angiotensin receptor blockers improved these abnormalities.