在人类冠状动脉微动脉中, ангиотензин II 型 2 型受体介导的血管扩张
Wendy W Batenburg1, Ingrid M Garrelds, Catherine Chapuis Bernasconi
1Department of Pharmacology, Erasmus MC, Rotterdam, The Netherlands.
Circulation
|May 1, 2004
概括
ангиотензин II 2型受体刺激会导致人体冠状动脉微动脉的血管扩张,由布拉迪基宁B2受体和氧化介导. 这种效应在老年人中更为明显.
科学领域:
- 心血管生理学心血管生理学
- 药理学 药理学是指药理学的学科.
- 分子生物学分子生物学
背景情况:
- ангиотензин II 2 型 (AT2) 受体的刺激会在老鼠中引起冠状动脉血管扩张.
- 在人类的大型冠状动脉中,AT2受体介导的血管扩张不存在.
- 人类冠状动脉微动脉 (HCMA) 中AT2受体的作用尚不清楚.
研究的目的:
- 为了研究人类冠状动脉微动脉 (HCMAs) 中安坦素II (Ang II) 诱导的血管扩张.
- 确定参与HCMA中AT2受体介导作用的受体通路.
- 评估供体年龄对AT2受体功能的影响.
主要方法:
- 来自49名心脏膜捐赠者的HCMAs被使用.
- 使用Mulvany myographs评估了血管功能.
- 测量了Ang II诱导的血管收缩和放松.
- 使用了受体对抗剂 (伊布沙坦,PD123319),氧化合成酶抑制剂 (L-NAME) 和布拉迪基宁B2受体对抗剂 (Hoe140).
- 放射性干结合和RT-PCR证实了AT2受体表达.
主要成果:
- 格II通过格II型1受体引起了HCMAs的度依赖收缩.
- 用PD123319阻断AT2受体增强了Ang II诱导的收缩,表明AT2受体具有血管扩张作用.
- 当Ang II型1受体被阻断时,Ang II在预先收缩的HCMA中诱导放松.
- 这种放松取决于布拉迪基宁B2受体,氧化和内皮.
- PD123319对Ang II诱导的收缩的增强作用随着供体年龄的增加而增加.
结论:
- 通过AT2受体介导的血管扩张发生在人类冠状动脉微动脉中.
- 这种血管扩张涉及布拉迪基宁B2受体和氧化,可能会作用于内皮细胞.
- 在人类中,AT2受体介导血管扩张的贡献随着年龄的增长而增加.
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