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脑肾素-血管紧张素系统:细胞间相互作用的分子机制

The brain renin-angiotensin system: molecular mechanisms of cell to cell interactions.

作者信息

Lippoldt A, Paul M, Fuxe K, Ganten D

机构信息

Max-Delbrück-Center for Molecular Medicine (MDC) Berlin-Buch, FRG.

出版信息

Clin Exp Hypertens. 1995 Jan-Feb;17(1-2):251-66. doi: 10.3109/10641969509087069.

Abstract

The components of the Renin-Angiotensin System (RAS) have been found to be expressed in the brain. Angiotensinogen, the high molecular weight precursor of the system, is widely distributed and expressed in areas not related to control of blood pressure and body fluid homeostasis as well. It has been shown that it is regulated by steroid hormones independently from the liver and that it is also regulated in a different manner in several brain areas. Angiotensin II, the effector peptide of the system, may be generated in the brain via the classical pathway, using renin and angiotensin converting enzyme or directly from angiotensinogen by cathepsin G or tonin. N-terminal peptides of angiotensin II have been found in several brain areas with ANG (1-7) involved in vasopressin release however without influence on blood pressure and with ANG III acting as potent as ANG II. Transgenic animals may be used to study the pathophysiology of an activated brain RAS.

摘要

肾素-血管紧张素系统(RAS)的组成成分已被发现存在于大脑中。血管紧张素原作为该系统的高分子量前体,广泛分布并表达于与血压控制和体液平衡无关的区域。研究表明,它受甾体激素调节,独立于肝脏,且在几个脑区也以不同方式受到调节。该系统的效应肽血管紧张素II可通过经典途径在大脑中生成,即利用肾素和血管紧张素转换酶,或直接由组织蛋白酶G或胰蛋白酶从血管紧张素原生成。在几个脑区已发现血管紧张素II的N端肽,其中ANG(1-7)参与抗利尿激素释放,但对血压无影响,而ANG III的作用与ANG II相当。转基因动物可用于研究激活的脑RAS的病理生理学。

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