首页> 外文期刊>Hypertension: An Official Journal of the American Heart Association >Blood pressure-independent cardiac hypertrophy induced by locally activated renin-angiotensin system.
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Blood pressure-independent cardiac hypertrophy induced by locally activated renin-angiotensin system.

机译:局部激活的肾素-血管紧张素系统诱发的非血压依赖性心脏肥大。

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摘要

Cardiac hypertrophy is frequent in chronic hypertension. The renin-angiotensin system, via its effector angiotensin II (Ang II), regulates blood pressure and participates in sustaining hypertension. In addition, a growing body of evidence indicates that Ang II acts also as a growth factor. However, it is still a matter of debate whether the trophic effect of Ang II can trigger cardiac hypertrophy in the absence of elevated blood pressure. To address this question, transgenic mice overexpressing the rat angiotensinogen gene, specifically in the heart, were generated to increase the local activity of the renin-angiotensin system and therefore Ang II production. These mice develop myocardial hypertrophy without signs of fibrosis independently from the presence of hypertension, demonstrating that local Ang II production is important in mediating the hypertrophic response in vivo.
机译:心脏肥大在慢性高血压中很常见。肾素-血管紧张素系统通过其效应器血管紧张素II(Ang II)调节血压并参与维持高血压。此外,越来越多的证据表明,Ang II也是一种生长因子。然而,在没有高血压的情况下,Ang II的营养作用是否会引发心脏肥大仍是一个有争议的问题。为了解决这个问题,产生了在大鼠心脏中过表达大鼠血管紧张素原基因的转基因小鼠,以增加肾素-血管紧张素系统的局部活性,从而增加Ang II的产生。这些小鼠独立于高血压的存在而发展成心肌肥大,而没有纤维化的迹象,表明局部Ang II产生在介导体内肥大反应中很重要。

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