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ангиотензин II 诱导的高血压在apoE缺乏的小鼠中加速动脉样硬化的发展

D Weiss¹, J J Kools, W R Taylor

¹Division of Cardiology, Department of Medicine, Atlanta VA Medical Center and Emory University School of Medicine, Atlanta, GA 30322, USA.

|February 7, 2001

概括

ангиотензин II (Ang II) 在apolipoprotein E缺陷 (apoE-/-) 的小鼠中显著加快动脉样硬化发展. 无论饮食如何,都观察到这种效应,突出了Ang II II.

科学领域:

心血管研究研究心血管研究
动脉样硬化的动物模型
高血压研究高血压研究

背景情况:

ангиотензин II (Ang II) 具有促进生长和促进炎症的特性.
这些效应表明Ang II在动脉样硬化病变的发展和进展中的潜在作用.

研究的目的:

为了调查Ang II诱导的高血压是否会加剧和加速阿波利波蛋白E缺陷 (apoE-/-) 的小鼠中的动脉样硬化.
为了确定Ang II对病变发展的特定影响,独立于饮食.

主要方法:

在8周的时间里,用透式迷你给apoE-/-小鼠服用Ang II (0.7 mg x kg(-1) x d(-1) SC).
小鼠被维持在标准食或异质性饮食上.
在下降的胸腔,腹腔和上升的大动脉中量化动脉样性损伤区域.

主要成果:

动脉样性损伤面积在接受动脉样性饮食的apoE-/-小鼠 (5.2+/-1.2%) 与标准 (0.4+/-0.1%) 相比显著更高.
在标准食 (11.0+/-2.3%) 的小鼠中,Ang II 治疗显著增加了病变面积,而在动性饮食 (69.9+/-9.4%) 的小鼠中,这一比例更高.
在接受标准食的小鼠中,Ang II显著增加了840+/-83μm2的损伤面积,在高脂肪饮食中增加了217+/-19μm2,而因诺阿基因林诱导的高血压则具有适度的影响.

结论:

ангиотензин II 诱导的高血压特别促进了apoE淘汰赛小鼠的动脉样硬化发展.
这种Ang II的亲动脉增生效应在标准饮食和动脉增生饮食的小鼠中明显.
这些研究强调了Ang II在加速动脉样硬化进展中的重要作用.

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