Fyhrquist F, Metsärinne K, Tikkanen I
Unit of Clinical Physiology, Minerva Institute for Medical Research, University of Helsinki, Finland.
J Hum Hypertens. 1995 Nov;9 Suppl 5:S19-24.
Angiotensin II (Ang II) raises blood pressure (BP) by a number of actions, the most important ones being vasoconstriction, sympathetic nervous stimulation, increased aldosterone biosynthesis and renal actions. Other Ang II actions include induction of growth, cell migration, and mitosis of vascular smooth muscle cells, increased synthesis of collagen type I and III in fibroblasts, leading to thickening of the vascular wall and myocardium, and fibrosis. These actions are mediated by type 1 Ang II receptors (AT1), and may be blocked by losartan, a specific blocker of AT1 receptors. In particular, studies employing losartan have shown that Ang II is an important contributor to BP regulation and plays a significant role in hypertension and in the pathophysiology of vascular damage during the course of hypertension. Ang II is also involved in the process of atherosclerosis and in remodelling and repair processes of the myocardium following myocardial infarction. Finally, increased Ang II is an important part of neurohumoral activation in heart failure. Exciting new discoveries concerned with polymorphisms of genes coding for angiotensin converting enzyme (ACE) and angiotensinogen suggest that Ang II may be genetically associated with increased risk for myocardial infarction, hypertension and left ventricular hypertrophy.
血管紧张素II（Ang II）通过多种作用升高血压（BP），其中最重要的作用是血管收缩、交感神经刺激、醛固酮生物合成增加和肾脏作用。Ang II的其他作用包括诱导血管平滑肌细胞生长、迁移和有丝分裂，增加成纤维细胞中I型和III型胶原蛋白的合成，导致血管壁和心肌增厚以及纤维化。这些作用由1型Ang II受体（AT1）介导，并且可能被氯沙坦（一种AT1受体特异性阻滞剂）阻断。特别是，使用氯沙坦的研究表明，Ang II是血压调节的重要因素，在高血压以及高血压病程中血管损伤的病理生理学中起重要作用。Ang II还参与动脉粥样硬化过程以及心肌梗死后心肌的重塑和修复过程。最后，Ang II增加是心力衰竭中神经体液激活的重要组成部分。与编码血管紧张素转换酶（ACE）和血管紧张素原的基因多态性有关的令人兴奋的新发现表明，Ang II可能在基因上与心肌梗死、高血压和左心室肥厚的风险增加相关。
