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高胆固醇血症刺激血管素合成,并通过AT1A受体促进动脉样硬化

Alan Daugherty¹, Debra L Rateri, Hong Lu

¹Division of Cardiovascular Medicine, Wethington Building, Room 521, University of Kentucky, Lexington, KY 40536-0200, USA. alan.daugherty@uky.edu

|December 15, 2004

概括

高胆固醇血症通过增加血管酶来加剧动脉样硬化. 阻止AT1A受体显著降低了这种效应,揭示了疾病进展的关键机制.

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.
动脉样硬化研究动脉样硬化研究

背景情况:

高胆固醇血引起的动脉样硬化因AT1受体对抗或缺乏而减弱.
血管激素II (Ang II) 反对作用的显著影响背后的机制尚不清楚.
这项研究调查了高胆固醇血是否会增加血管素的产生,从而解释AT1A受体缺乏的影响.

研究的目的:

确定AT1A受体缺乏对动脉样硬化的明显影响背后的机制.
为了调查高胆固醇血症是否刺激血管素的产生.
为了确定AT1A受体缺乏对动脉动脉产生所观察到的影响的理由.

主要方法:

在LDL受体缺乏的小鼠中的动脉样硬化病变的分析.
免疫细胞化学分析以确定病变内的Ang II合成途径的组成部分.
在野生型和缺少AT1A受体的小鼠中评估病变大小,组成,缩血压,氧化和化学吸引剂.
测量大动脉AT2受体mRNA表达和AT2受体缺陷的影响.
在高胆固醇和AT1A受体缺乏的小鼠中的血血管新生素和血管新生素的量化.

主要成果:

在雄性和雌性小鼠中,AT1A受体缺陷显著降低了动脉样损伤的大小.
动脉样硬化的减少独立于血压,氧化和化学吸引剂.
高胆固醇血症显著增加了全身 ангиотензиноген和 ангиотензин (Ang II, III, IV, 4-8).
在高胆固醇的AT1A受体缺乏的小鼠中,血管素的这些增加被废除了.
AT2受体表达和缺乏并没有显著影响病变区域或组成.

结论:

在LDL受体阴性小鼠中,AT1A受体缺乏明显降低了高胆固醇血引起的动脉样硬化.
高胆固醇血症与系统性血管酶的增加有关.
AT1A受体缺乏减轻了高胆固醇血引起的血管酶的增加.
这项研究表明,高胆固醇血刺激了血管素的产生,这解释了AT1A受体缺乏在减少动脉样硬化方面的显著益处.

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