神经Y与同情神经系统在人体血管控制中的相互作用
J Clarke1, N Benjamin, S Larkin
1Department of Cardiovascular Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.
Circulation
|March 1, 1991
概括
神经Y (NPY) 强烈地直接收缩人类前臂血管,独立于α受体. 这项研究发现NPY不会影响诺亚上腺素.
科学领域:
- 心血管生理学心血管生理学
- 自主神经系统的调节规则
- 血管药理学 血管药理学
背景情况:
- 神经Y (NPY) 涉及到循环的自主控制.
- 在交感神经中,NPY与诺亚上腺素共存,并缩小血管床.
- 在体外,NPY的血管效应是直接或间接通过诺亚上腺素调节,但体内相关性尚不清楚.
研究的目的:
- 为了研究NPY对人类前臂血管抵抗的体内影响.
- 为了确定NPY是否在体内调节诺拉上腺素的血管缩作用.
主要方法:
- 在6名志愿者身上进行了动脉内NPY输液.
- 与诺拉丁上腺素同时输注,并在下体负压 (LBNP) 期间评估反射交感刺激.
- 评估NPY的效果与或没有α-阻断剂 (芬托胺).
主要成果:
- NPY导致前臂血流量剂量依赖的减少 (最大49%).
- NPY并没有改变输入诺亚上腺素或反射交感刺激的血管收缩反应.
- NPY的血管收缩作用独立于α受体,因为它在托胺阻塞后持续存在.
结论:
- NPY是人类前臂阻力血管的强有力的收缩剂,通过直接的,α受体独立的机制.
- NPY不会调节内源性或输注的诺亚上腺素的体内血管收缩作用.
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