在II型糖尿病患者中,内源性内甲林活性增加
Carmine Cardillo1, Umberto Campia, Melissa B Bryant
1Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md, USA.
Circulation
|October 3, 2002
概括
在糖尿病患者的血管中,内甲素-1 (ET-1) 对ET(A) 受体的活性增加,而对ET-1的敏感性降低. 这可能会导致糖尿病的血管并发症.
科学领域:
- 心血管研究研究心血管研究
- 内分泌学 在内分泌学.
- 血管生物学 血管生物学
背景情况:
- 内皮功能障碍与糖尿病中的动脉样硬化有关.
- 恩多林-1 (ET-1) 可能促进光滑肌肉细胞线粒发生和白细胞粘附.
- 在II型糖尿病中研究内源性ET-1活性至关重要.
研究的目的:
- 用ET-1受体抗剂评估II型糖尿病患者内源性ET-1活性.
- 为了比较糖尿病患者和对照者之间对ET-1受体阻塞和外源ET-1的前臂血流 (FBF) 反应.
主要方法:
- 前臂血流 (FBF) 响应使用张力表囊造影法进行测量.
- 选择性ET(A) 受体阻塞 (BQ-123) 和ET-1输注进行了静脉内输注.
- 15名糖尿病患者和12名健康对照人群进行了比较.
主要成果:
- 与对照组不同的是,BQ-123在糖尿病患者中诱导了显著的血管扩张.
- 外源ET-1导致糖尿病患者与对照人群相比,血管收缩.
- 在这两组中,上腺素血管收缩剂的反应是相似的.
结论:
- 在糖尿病耐药性血管中,内源性ET-1在ET(A) 受体上的活性得到增强.
- 糖尿病患者对外源ET-1的敏感性降低.
- 这些ET-1通路异常可能导致糖尿病血管并发症.
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