ROLE OF THE RENIN-ANGIOTENSIN SYSTEM IN OBESITY-RELATED ENDOTHELIAL DYSFUNCTION

肾素-血管紧张素系统在肥胖相关内皮功能障碍中的作用

• 批准号: 7377894
• 负责人: Demetra Christou
• 金额: $ 3.96万
• 依托单位: UNIVERSITY OF COLORADO DENVER
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-04-01 至 2007-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7377894
• 关键词: ROLE; RENIN; ANGIOTENSIN; SYSTEM; OBESITY

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Flow-mediated dilation (FMD) reflects the ability of the vascular endothelium to produce vasodilation in response to physiological increases in blood flow. It is primarily mediated by the release of vascular endothelium derived nitric oxide (NO). Brachial FMD is reduced in many types of cardiovascular diseases (CVD). Brachial FMD correlates with coronary vascular endothelial function and predicts future cardiovascular events in patients with CVD. FMD is also impaired in individuals with high intra-abdominal fat, which may contribute to the increased prevalence of CVD in these individuals. Therefore, identifying the mechanisms involved in the impairment of brachial FMD with abdominal visceral obesity has important clinical implications. Experimental evidence suggests that angiotensin II-induced oxidative stress plays a critical role in impaired FMD in patients with cardiovascular diseases. Because abdominal visceral obesity is also associated with increased oxidative stress levels, it is possible that at least part of the increased oxidative stress within the arterial wall seen with obesity may be due to an increased formation of ROS by angiotensin II, contributing to the obesity-related decline in FMD. Consequently, the specific aim of this study is to measure FMD before and after acute angiotensin II type 1 receptor blockade with Candesartan in men and women with high and low abdominal visceral fat.

该子项目是利用 NIH/NCRR 资助的中心拨款提供的资源的众多研究子项目之一。子项目和研究者 (PI) 可能已从另一个 NIH 来源获得主要资金，因此可以在其他 CRISP 条目中得到体现。列出的机构是中心的机构，不一定是研究者的机构。血流介导的扩张（FMD）反映了血管内皮响应血流生理增加而产生血管舒张的能力。它主要由血管内皮衍生的一氧化氮（NO）的释放介导。许多类型的心血管疾病 (CVD) 中的肱动脉 FMD 都会减少。肱动脉 FMD 与冠状血管内皮功能相关，可预测 CVD 患者未来的心血管事件。腹内脂肪高的个体的 FMD 也会受到损害，这可能导致这些个体中 CVD 患病率的增加。因此，确定腹部内脏肥胖引起的肱动脉FMD损伤的机制具有重要的临床意义。 实验证据表明，血管紧张素 II 诱导的氧化应激在心血管疾病患者的 FMD 受损中发挥着关键作用。由于腹部内脏肥胖也与氧化应激水平增加有关，因此肥胖引起的动脉壁内氧化应激增加的至少一部分可能是由于血管紧张素 II 形成的 ROS 增加，从而导致肥胖。 FMD 相关下降。因此，本研究的具体目的是测量具有高和低腹部内脏脂肪的男性和女性使用坎地沙坦急性血管紧张素 II 1 型受体阻断前后的 FMD。