Mechanism of the central angiotensin-induced sympatho-modulatory effect

中枢血管紧张素诱导交感神经调节作用的机制

基本信息

批准号：
13670059
负责人：
SAIGUSA Takeshi
金额：
$ 2.24万
依托单位：
University of Yamanashi (Faculty of Medicine)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2002
项目状态：
已结题

项目摘要

Fourth-ventricular (4V) administration of angiotensin II (Ang II) facilitates renal sympathetic baroreflex in rabbits. The aim of the present study is to identify the site(s) of this Ang II action and to clarify its neuronal mechanism.1. Identifying the site of actionThe renal sympathetic baroreflex facilitation induced by 4V Ang II (10 pmol/min) was completely blocked by a pretreatment of bilateral rostral ventrolateral medulla (RVLM) with an Ang II receptor antagonist (Sarile, 10 pmol). The result strongly suggests that the RVLM is the major site of action mediating the 4V Ang II-induced baroreflex facilitation.2. Development of a unit-recording systemA new recording system was developed for the purpose of recording single-unit activities from the medullary cardiovascular neurons during baroreflex analysis. The system consists of a carbon-fiber floating electrode and an electrode tracking-control device that compensates brain dislocation induced by blood pressure manipulation.3. Clarifying the neuronal mechanismThe effects of Ang II on the blood pressure-activity relationship of the RVLM cardiovascular neurons were investigated. In half of the cardiovascular neurons investigated, Ang II increased the upper limit of neuronal activation in response to a decrease in blood pressure. Average curves before and after the Ang II administration were reconstructed from the individual blood pressure-activity relationships. The average curves were qualitatively identical with the renal sympathetic baroreflex curves before and after 4V Ang II. The result suggests that the 4V Ang II-induced sympathetic baroreflex modulation is attributed to the effects of Ang II on the blood pressure-activity relationship in the RVLM cardiovascular neurons.

血管紧张素II（ANG II）的第四腹膜（4V）促进兔子中的肾交感上的压力反射。本研究的目的是识别此ANG II作用的部位，并阐明其神经元机制1。识别作用部位，由4V ANG II（10 pmol/min）诱导的肾交感交感神经反射促进作用被双边腹侧腹侧髓质（RVLM）和Ang II受体拮抗剂（Sarile，10 pmol）进行了经过治疗。结果强烈表明RVLM是介导4V ANG II诱导的压力反射促进的主要作用部位。2。开发单位录制系统新记录系统的开发是为了在BaroreFlex分析期间从髓质心血管神经元记录单单元活动。该系统由碳纤维浮动电极和一个电极跟踪控制装置组成，该设备补偿了由血压操纵引起的大脑脱位3。研究了ANG II对RVLM心血管神经元血压活性关系的影响。在研究的一半心血管神经元中，ANG II因血压降低而增加了神经元激活的上限。 ANG II前后给药前后的平均曲线是从单个血压活性关系中重建的。在4V ANG II之前和之后，平均曲线与肾交感上的压力反射曲线在质量上相同。结果表明，4V ANG II诱导的交感神经反射调制归因于ANG II对RVLM心血管神经元血压活性关系的影响。