在高血压患者中通过内源性交感激活减少心脏 natriuretic 因素的循环水平
1Istituto di 1 Clinica Medica, 2 Facoltà di Medicina, Università di Napoli, Italy.
Circulation
|May 1, 1988
概括
在高血压患者中,交感神经系统的激活会减少心房 natriuretic 因子 (ANF) 的释放,独立于心房壁的张力. 这一发现表明同情活动与高血压中的ANF水平之间存在直接联系.
科学领域:
- 心血管生理学心血管生理学
- 内分泌学 在内分泌学.
背景情况:
- 基本高血压的特点是同情神经系统活动的改变.
- 在心血管恒温中,心房性尿素因子 (ANF) 起着至关重要的作用.
- 在高血压中,交感激活和ANF释放之间的相互作用需要进一步阐明.
研究的目的:
- 研究内源交感神经系统激活对系统和区域血液动力学的影响.
- 为了检查交感激活对心房性尿素因子 (ANF) 在基本高血压中的血水平的影响.
- 为了确定除了心房壁紧张之外的其他因素是否会在交感刺激期间影响ANF释放.
主要方法:
- 在高血压患者中,通过使用部腔室增加外部部组织压力 (NTP) 来诱导反射交感神经系统激活.
- 用分级和持续水平的NTP来评估剂量依赖和时间效应.
- 测量了血液动力学参数 (血压,心率,前臂血管阻力,心输出,心房压力) 和血免疫反应性ANF (irANF) 水平.
- 用上腺体阻塞来证实交感通路的作用.
主要成果:
- NTP诱导的反射增加了血压,心率和前臂血管阻力,心房压力没有显著变化.
- 血irANF水平随着NTP的增加而逐渐降低,显示出与前臂血管抵抗的显著负相关性.
- 血液动力学和irANF的变化被联合上腺体阻塞取消,证实了同情调解.
- 持续的NTP导致肺动脉和下静脉中irANF水平降低,动脉静脉差异减少.
结论:
- 在高血压患者中,内源性交感神经系统激活可以减少ANF释放.
- 这些发现表明,除了心房壁拉伸之外的因素,如同情驱动,会影响高血压中ANF分泌.
- 这项研究突出了一个新的机制,通过这种机制,交感过度活动可能会导致高血压的病理生理学.
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