在动脉样硬化的子冠状动脉中,通过5-基三胺1B受体引起的血清激素过度收缩
T Ishida1, S Kawashima, Hirata Ki
1First Department of Internal Medicine and Institute for Experimental Animals, Kobe (Japan) University School of Medicine.
Circulation
|March 10, 2001
概括
动脉样硬化会增加子冠状动脉中血清素诱导的收缩,主要是通过升调的5-HT(1B) 受体. 这种机制涉及加强动员,并有助于心肌缺血.
科学领域:
- 心血管生物学 心血管生物学
- 药理学 药理学是指药理学的学科.
- 动脉样硬化研究 动脉样硬化研究
背景情况:
- 在动脉样硬化血管中增加了对血清素 (5-hydroxytryptamine [5-HT]) 的血管收缩,导致心肌缺血.
- 研究了动脉样硬化冠状动脉中血清醇引起的超收缩背后的机制.
研究的目的:
- 阐明导致动脉样硬化冠状动脉中增强的血清激素诱导血管收缩的机制.
- 为了确定特定的血清素受体亚型和参与这种超收缩的信号通路.
主要方法:
- 从对照和Watanabe遗传性高脂血症 (WHHL) 子中检查了内皮脱皮冠状动脉对血清激素剂的收缩反应.
- 使用了5-HT ((1B/1D) 和5-HT ((2) 受体对抗剂,百日咳毒素,并测量了细胞内 ([Ca ((2+) ]) 和mRNA水平.
主要成果:
- WHHL冠状动脉对5-HT(1) -受体激动剂呈现高收缩,值度较低,最大反应增加.
- 血清激素引起的收缩被5-HT (((1B/1D) 抗剂和百日咳毒素抑制,但不是5-HT (((2) 抗剂.
- 过度收缩与增强的[Ca2+]升高相关,在WHHL动脉中,5-HT1B) mRNA水平显著上调.
结论:
- 动脉样硬化冠状动脉表现出增强的收缩和调动,以应对血清素.
- 在动脉样硬化中被上调的5-HT1B受体是血清素增强作用的可能媒介.
- 这些发现突显了5-HT(1B) 受体上调的作用在动脉样硬化期间的中介血管收缩中.
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