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Guido Iaccarino¹, Michele Ciccarelli, Daniela Sorriento

¹Department of Clinical Medicine, University of Naples Federico II, Italy. guiaccar@unina.it

|May 12, 2004

概括

在高血压中,受损的AKT激酶局部化有助于内皮功能障碍. 在自发高血压的老鼠中恢复AKT1基因表达使血管功能正常化,这表明了治疗点.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
高血压研究高血压研究

背景情况:

高血压与氧化产量减少和内皮血管扩张受损有关.
AKT激酶酸化并激活内皮氧化合成酶;其功能障碍可能是内皮功能障碍的基础.

研究的目的:

研究AKT激酶在 normotensive Wistar-Kyoto大鼠 (WKY) 和自发高血压大鼠 (SHR) 内皮功能中的生理作用.
为了确定AKT1基因转移是否可以改善自发高血压大鼠的内皮功能障碍.

主要方法:

使用腺病毒载体将人类AKT1基因输送到WKY和SHR的动脉内皮.
在实验室内对乙胆,异二醇和胰岛素的内皮依赖性血管松反应进行了评估.
通过多普勒超声波测量体内 carotid 血流量.
在培养的内皮细胞中检查了AKT酸化,活性和细胞局部化.

主要成果:

与WKY大鼠相比,SHR中的内皮血管松减弱,而AKT1基因转移使这些反应正常化.
在活体上,在AKT1基因转移后,心血管血流在SHR下降并恢复到WKY水平.
与WKY大鼠相比,来自SHR的内皮细胞表现出AKT激酶的错位化.

结论:

在自发高血压的老鼠中,AKT的膜局部受损会导致内皮功能障碍.
AKT在与高血压相关的内皮功能障碍的病理生理学中发挥着重要作用.

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