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首页> 外文期刊>Therapeutic advances in cardiovascular disease. >Cardiac remodelling and RAS inhibition
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Cardiac remodelling and RAS inhibition

机译：心脏重塑和RAS抑制

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Risk factors such as hypertension and diabetes are known to augment the activity and tissue expression of angiotensin II (Ang II), the major effector peptide of the renin–angiotensin system (RAS). Overstimulation of the RAS has been implicated in a chain of events that contribute to the pathogenesis of cardiovascular (CV) disease, including the development of cardiac remodelling. This chain of events has been termed the CV continuum. The concept of CV disease existing as a continuum was first proposed in 1991 and it is believed that intervention at any point within the continuum can modify disease progression. Treatment with antihypertensive agents may result in regression of left ventricular hypertrophy, with different drug classes exhibiting different degrees of efficacy. The greatest decrease in left ventricular mass is observed following treatment with angiotensin converting enzyme inhibitors (ACE-Is), which inhibit Ang II formation. Although ACE-Is and angiotensin receptor blockers (ARBs) provide significant benefits in terms of CV events and stroke, mortality remains high. This is partly due to a failure to completely suppress the RAS, and, as our knowledge has increased, an escape phenomenon has been proposed whereby the human sequence of the 12 amino acid substrate angiotensin-(1-12) is converted to Ang II by the mast cell protease, chymase. Angiotensin-(1-12) is abundant in a wide range of organs and has been shown to increase blood pressure in animal models, an effect abolished by the presence of ACE-Is or ARBs. This review explores the CV continuum, in addition to examining the influence of the RAS. We also consider novel pathways within the RAS and how new therapeutic approaches that target this are required to further reduce Ang II formation, and so provide patients with additional benefits from a more complete blockade of the RAS.
机译：已知诸如高血压和糖尿病等危险因素会增强血管紧张素II（Ang II）的活性和组织表达，血管紧张素II是肾素-血管紧张素系统（RAS）的主要效应肽。 RAS过度刺激与一系列事件有关，这些事件导致心血管（CV）疾病的发病机理，包括心脏重塑的发展。这一系列事件被称为简历连续体。作为连续体存在的CV疾病的概念是在1991年首次提出的，并且认为在连续体中的任何点进行干预都可以改变疾病的进展。用降压药治疗可能导致左心室肥大消退，不同的药物类别表现出不同程度的疗效。在用血管紧张素转化酶抑制剂（ACE-Is）治疗后，观察到左心室质量的最大减少，该抑制剂可抑制Ang II的形成。尽管ACE-Is和血管紧张素受体阻滞剂（ARB）在CV事件和中风方面具有显着优势，但死亡率仍然很高。这部分是由于无法完全抑制RAS，并且，随着我们的知识的增加，提出了一种逃逸现象，通过该逃逸现象，人的12个氨基酸底物血管紧张素-（1-12）的序列会通过以下方式转化为Ang II：肥大细胞蛋白酶，糜酶。血管紧张素-（1-12）在广泛的器官中含量丰富，在动物模型中已显示会增加血压，这种作用因ACE-Is或ARB的存在而被消除。除了审查RAS的影响之外，本次审查还探讨了CV连续体。我们还考虑了RAS内的新途径，以及如何需要针对此的新治疗方法以进一步减少Ang II的形成，从而为患者提供了更完全阻断RAS的额外益处。

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