膜拉伸和血管紧张素II型1a受体:致肌反应的原因和作用

J. Tano, J. Schleifenbaum, M. Gollasch
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引用次数: 0

摘要

血管紧张素II型1受体在血管拉伸后的非配体激活起着非常重要的(病理)生理作用。事实上,最近的研究表明,这种机制在压力过载条件下的心脏肥厚中起作用,并且在小阻力动脉、肠系膜和肾阻力动脉的平滑肌细胞的肌生成反应的调节中发挥着不可或缺的作用。这里讨论的信息将强调血管紧张素II型受体的机械激活参与肌生成反应的发展,以及激活后调节它们的分子机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Membrane stretch and angiotensin II type 1a receptor: causes and role in the myogenic response
The ligand-independent activation of Angiotensin II type 1 receptors following vascular stretch plays very important (patho) physiological roles. Indeed, recent studies have implicated this mechanism in cardiac hypertrophy under conditions of pressure overload and it has shown to be indispensable in the regulation of the myogenic response in smooth muscle cells of small resistance arteries, as well as mesenteric and renal resistance arteries. The information discussed in here will highlight the involvement of the mechanoactivation of the Angiotensin II type I receptors in the development of the myogenic response and the molecular mechanisms modulating them following activation.
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