阿尔多斯特通过血管激素II依赖途径增强缺血诱导的新血管化
Frédéric Michel1, Marie-Lory Ambroisine, Micheline Duriez
1INSERM U541, Hôpital Lariboisière, IFR Circulation-Lariboisière, Université Paris, Paris, France.
Circulation
|April 14, 2004
概括
阿尔多激素通过激活血管激素II (Ang II) 途径,促进缺血四肢的新血管生长. 阻断Ang II类型1受体消除了这种效应,突出了它在阿尔多斯激素诱导的新血管化中的关键作用.
科学领域:
- 心血管生物学 心血管生物学
- 内分泌学 在内分泌学.
- 血管生物学 血管生物学
背景情况:
- 研究阿尔多在缺血引起的新血管化的作用.
- 检查血管素II (Ang II) 信号传递对阿尔多素对血管生长的影响的参与.
研究的目的:
- 为了确定阿尔多是否增强了缺血症后的新血管化.
- 阐明特定的信号通路,特别是Ang II,调解阿尔多的益血管效应.
主要方法:
- 在小鼠后肢中通过股骨动脉绑定诱导缺血.
- 服用阿尔多素,螺旋龙 (阿尔多素受体阻断剂) 或瓦尔萨坦 (Ang II类型1受体阻断剂).
- 使用微血管学,毛细血管密度,激光多普勒输液和VEGF蛋白质分析评估新血管化.
主要成果:
- 在缺血性小鼠中,阿尔多斯特治疗显著改善了新血管和四肢 perfusion.
- 阿尔多斯特增加了血管内皮生长因子 (VEGF) 蛋白质水平.
- 阻断Ang II类型1受体消除了阿尔多的益血管性作用,而血管激素 mRNA增加.
结论:
- 阿尔多斯特在缺血性疾病中刺激新血管化.
- 这种效应通过激活Ang II信号通路来实现.
- 阿尔多可能会将Ang II信号的平衡转移到亲血管性结果.
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