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[心脏肥大与大动脉干变化之间的关系。肾素-血管紧张素系统的作用]

[Relation between cardiac hypertrophy and changes in the large arterial trunks. Role of the renin-angiotensin system].

作者信息

Benetos A

机构信息

Hôpital Broussais, laboratoire de pharmacologie, U337, Paris.

出版信息

Arch Mal Coeur Vaiss. 1995 Feb;88 Spec No 2:21-4.

PMID:7646306
Abstract

The raised mean arterial pressure observed in hypertension increases the stress on the walls of large arteries by increasing the mechanical forces to which they are submitted. Cardiac and arterial wall hypertrophy seem to be adaptive mechanisms tending to reduce the stress in each musculo-elastic unit of the cardiovascular system. However, this adaptation only partially explains the development of cardiovascular hypertrophy. Cardiovascular changes are sometimes observed before the increase in blood pressure, as in normotensive children of hypertensive parents. Moreover, a dissociation has been shown between the antihypertensive effects of different antihypertensive agents. For the same reduction in mean arterial pressure, some drugs are associated with a greater regression in these changes than others. At present, it is acknowledged that other factors than mean arterial pressure may cause these changes. For example, the pulse pressure is a major factor, independent of mean arterial pressure, in developing cardiovascular hypertrophy. The activation of hormonal systems, especially the angiotensin converting enzyme system, influences cardiovascular structure. Therefore, hyperactivity of the renin-angiotensin system may stimulate the growth factor responsible for cardiac and arterial hypertrophy.

摘要

高血压患者中观察到的平均动脉压升高,通过增加大动脉壁所承受的机械力,加大了大动脉壁的压力。心脏和动脉壁肥厚似乎是适应性机制,倾向于降低心血管系统每个肌肉弹性单元的压力。然而,这种适应性只能部分解释心血管肥厚的发展。心血管变化有时在血压升高之前就已出现,比如高血压患者的血压正常的子女。此外,不同降压药的降压效果之间已显示出一种分离现象。对于相同程度的平均动脉压降低,一些药物与这些变化的更大程度的逆转相关,而另一些药物则不然。目前,人们认识到除平均动脉压之外的其他因素可能导致这些变化。例如,脉压是导致心血管肥厚的一个主要因素,独立于平均动脉压。激素系统的激活,尤其是血管紧张素转换酶系统,会影响心血管结构。因此,肾素 - 血管紧张素系统的过度活跃可能刺激负责心脏和动脉肥厚的生长因子。

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