交感神经活动亢进是高血压病的主要特征并与其发展和预后密切相关，交感中枢头端延髓腹外侧区（RVLM）氧化应激增强是高血压交感输出亢进的主要原因之一，抑制氧化应激已成为改善高血压心血管功能异常的重要策略。莫索尼定等中枢降压药物可激活RVLM的咪唑啉1型受体从而抑制交感活动，但其与氧化应激的关系并不明确。因此，本研究总体目标是阐明莫索尼定对RVLM氧化应激的作用机制及其在抗高血压中的意义，通过整体和分子生物学实验将明确： 1）高血压状态下莫索尼定是否降低RVLM内的氧化应激；2）莫索尼定是否抑制Ang II-AT1R-NADPH氧化酶通路从而降低RVLM内氧化应激的作用及机制；3）莫索尼定是否改善NOS脱偶联减少RVLM内氧化应激的作用及机制。通过以上研究将为阐明咪唑啉样药物的作用特点和意义提供重要的理论内容，对于揭示氧化应激在高血压发病机制中的作用和意义具有重要的理论和临床应用价值。

Sympathetic overactivity is the main feature of hypertension and takes an important role in its development and prognosis. The enhancement of oxidative stress in sympathetic center rostral ventrolateral medulla (RVLM) contributes to sympathetic overactivity, so the inhibition of oxidative stress has become an important strategy to improve hypertensive cardiovascular dysfunction . Moxonidine decreases sympathetic activity via activating central imidazoline type 1 receptor in the RVLM, but its relationship with oxidative stress is not clear. Thus , the globe goal of this study is to clarify the mechanism respossible for the effect of moxonidine on oxidative stress in the RVLM, and to further illustrate the significance of moxonidine action in reducing the sympathetic overactivity in hypertension. Using acute/chronic and molecular biological experiments in the model of spontensively hypertensive rats and CATH.a neurons, the project aims to: 1) to determine the action of moxonidine on the oxidative stress within RVLM in hypertension; 2) to determine the mechanism of moxonidine responsible for Ang II-AT1R-NADPH oxidase-induced oxidative stress in the RVLM; 3) to determine the effect of moxonidine on NOS uncoupling-induced oxidative stress in the RVLM. The new evidence obtained from this project will provide the important theoretical significance content for clarifying the effect and characteristics of imidazoline-like drugs, and also helpful for revealing the role and significance of oxidative stress in the pathogenesis of hypertension, which has important theoretical and clinical applications against cardiovascular diseases.