Rothermund L, Paul M
Freie Universität Berlin, Institute of Clinical Pharmacology and Toxicology, Germany.
Basic Res Cardiol. 1998;93 Suppl 2:1-6. doi: 10.1007/s003950050191.
The renin-angiotensin system (RAS) has been extensively studied in the past decades as an important mediator of hypertension and hypertensive end-organ damage. Originally, the RAS was described as an endocrine system that exerts its action through the effector peptide angiotensin II (ANG II). Recently, tissue-based renin-angiotensin systems which act through paracrine-autocrine mechanisms have been suggested as the more important pathway. After all, genes of the RAS have been cloned transgenic animals overexpressing different components of the RAS were constructed. Furthermore, gene polymorphisms were investigated as genetic markers for hypertension and cardiovascular disease. Finally, very effective substances interacting on different levels of the RAS cascade were developed.
在过去几十年中，肾素-血管紧张素系统（RAS）作为高血压及高血压性靶器官损害的重要介质，已得到广泛研究。最初，RAS被描述为一种通过效应肽血管紧张素II（ANG II）发挥作用的内分泌系统。最近，有人提出通过旁分泌-自分泌机制发挥作用的组织型肾素-血管紧张素系统是更为重要的途径。毕竟，RAS的基因已被克隆，并构建了过表达RAS不同组分的转基因动物。此外，还对基因多态性进行了研究，将其作为高血压和心血管疾病的遗传标记。最后，开发出了作用于RAS级联反应不同水平的非常有效的物质。
