在有意识的老子中,矛盾地增强了内甲素-B受体介导的血管收缩
1Cardiovascular Research Institute, University of Medicine, Dentistry of New Jersey, New Jersey Medical School, Newark, USA.
Circulation
|May 23, 2001
概括
老龄化会损害子对烯和血管素II的血管收缩反应. 然而,内素-1 (ET-1) 在老子中引起更大的血管收缩,这表明内依赖的血管扩张受损,涉及ET(B) 受体.
科学领域:
- 心血管生理学心血管生理学
- 衰老研究研究 衰老研究
- 药理学 药理学是指药理学的学科.
背景情况:
- 研究了衰老对有意识的老年和年轻成年子血管收缩反应的影响.
- 对内甲素 (ET), (PE) 和血管素II (Ang II) 的反应进行比较.
研究的目的:
- 为了确定衰老如何影响身体对内甲蛋白 (ET) 和其他血管收缩剂的反应.
- 在老年灵长类动物中阐明血管缩器敏感性改变背后的机制.
主要方法:
- 使用长期仪器意识的老年人 (19.8+/-0.6年) 和年轻成年人 (6.8+/-0.3年) .
- 使用的血管收缩剂:PE,Ang II,内甲素-1 (ET-1),以及一个ET(B) 受体激动剂 (sarafotoxin S6c) 与一个ET(A) 激动剂 (BQ-123).
- 利用氧化合成酶 (NOS) 抑制来评估内皮依赖血管扩张的作用.
主要成果:
- 与年轻子相比,在老子中减少了PE和Ang II的血管收缩.
- 在老子中显著增强了对ET-1的血管收缩.
- 在老子中,通过ET(B) 受体进行ET-1介导的血管收缩也得到了增强.
- 在老和年轻的子中,NOS抑制使ET-1介导的血管收缩正常化,这表明老年人体内皮依赖血管扩张受损.
结论:
- 随着年龄的增长,对PE和Ang II的外周血管收缩会减少.
- 矛盾的是,ET-1诱导的血管收缩在老子中得到增强.
- 这种增强归因于内皮依赖血管扩张的受损,可能涉及ET(B) 受体通路.
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