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在高血压和遗传倾向的正常血压受试者中,L-氨酸运输和内皮功能受损
Markus P Schlaich1, Melinda M Parnell, Belinda A Ahlers
1Wynn Department of Metabolic Cardiology, Baker Heart Research Institute, Melbourne, Victoria, Australia.
Circulation
|December 1, 2004
概括
损伤的L-氨酸运输与基本高血压有关,并预测高血压风险. 补充L-氨酸改善了高血压和家族病史患者的血管扩张.
科学领域:
- 心血管生理学心血管生理学
- 高血压病理生理学 高血压病理生理学
- 内皮细胞功能 内皮细胞功能
背景情况:
- 基本高血压的特征是受损的内皮依赖NO介导的血管扩张.
- 这种内皮功能障碍可能会在血压升高之前出现.
- 研究了L-氨酸运输在这个过程中的作用.
研究的目的:
- 为了研究L-氨酸运输和内皮功能障碍在基本高血压之间的关系.
- 评估高血压个体和健康个体的L-氨酸吸收,有或没有高血压家族病史.
- 为了确定L-氨酸补充剂是否可以改善风险人群的内皮功能.
主要方法:
- 利用放射性追踪器动力学 ([3H]L-氨酸) 来测量前臂和外围血液单核细胞的氨酸吸收.
- 评估前臂血流对乙胆和酸的反应.
- 在体内和体外测量L-氨酸运输,以及CAT-1表达和血ADMA水平.
主要成果:
- 在基本高血压和积极家族病史组中,L-氨酸的运输显著减少.
- 两组之间没有发现CAT-1mRNA/蛋白质或血L-氨酸/ADMA的差异.
- 静脉内L-氨酸仅在基本高血压和积极家族病史组中改善了乙胆反应.
结论:
- 患有高血压高风险的正常血压患者表现出L-氨酸运输受损,类似于高血压患者.
- 这种L-氨酸运输的缺陷可能会将L-氨酸/NO通路的缺陷与基本高血压的发展联系起来.
- 传输缺陷并不能通过改变CAT-1表达或增加ADMA水平来解释.
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