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生长还是抗生长:血管紧张素与内皮细胞

Growth or antigrowth: angiotensin and the endothelium.

作者信息

Stoll M, Meffert S, Stroth U, Unger T

机构信息

Department of Pharmacology, Christian Albrechts University of Kiel, Germany.

出版信息

J Hypertens. 1995 Dec;13(12 Pt 2):1529-34.

PMID:8903605
Abstract

AIM

Antihypertensive drugs that interfere with the renin-angiotensin system, such as angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor antagonists, are increasingly being perceived to exert effects beyond blood pressure control, for instance on vascular structure and function. In a recent study we demonstrated that early-onset treatment of spontaneously hypertensive rats with an ACE inhibitor induced an increase in myocardial capillary length density independently of the antihypertensive and antihypertrophic actions of the drug. The aim of the present work was to focus on the growth-modulating effects of angiotensin II on vascular cells and the differential role played by the two angiotensin II receptor subtypes, AT1 and AT2, in the regulation of cell growth and differentiation.

RESULTS

Recent findings indicate that angiotensin II exerts different growth-modulating actions depending on the presence or absence of angiotensin II receptor subtypes on a given cell. The growth-promoting effect of angiotensin II is mediated by the AT1 receptor and is associated with the increased expression of growth factors and immediate early genes. In endothelial cells, this effect is counteracted by the antiproliferative actions of the AT2 receptor. Angiotensin II may also be involved in the process of angiogenesis and development mediated by AT1 and AT2 receptors expressed in various tissues.

摘要

目的

干扰肾素 - 血管紧张素系统的抗高血压药物,如血管紧张素转换酶(ACE)抑制剂和血管紧张素II受体拮抗剂,越来越被认为具有超出血压控制的作用,例如对血管结构和功能的影响。在最近的一项研究中,我们证明用ACE抑制剂对自发性高血压大鼠进行早期治疗可使心肌毛细血管长度密度增加,且与该药物的降压和抗肥厚作用无关。本研究的目的是关注血管紧张素II对血管细胞的生长调节作用以及两种血管紧张素II受体亚型AT1和AT2在细胞生长和分化调节中所起的不同作用。

结果

最近的研究结果表明,血管紧张素II根据给定细胞上血管紧张素II受体亚型的存在与否发挥不同的生长调节作用。血管紧张素II的促生长作用由AT1受体介导,并与生长因子和即刻早期基因表达增加有关。在内皮细胞中,这种作用被AT2受体的抗增殖作用抵消。血管紧张素II也可能参与由各种组织中表达的AT1和AT2受体介导的血管生成和发育过程。

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