Hirsch A T, Pinto Y M, Schunkert H, Dzau V J
Cardiovascular Division, University of Minnesota Hospitals, Minneapolis 55455.
Am J Cardiol. 1990 Oct 2;66(11):22D-30D; discussion 30D-32D. doi: 10.1016/0002-9149(90)90473-e.
The circulating renin-angiotensin system (RAS) plays an important role in the maintenance of cardiovascular homeostasis. It has recently been demonstrated that endogenous RAS exist in target tissues that are important in cardiovascular regulation. This article reviews the multiple effects of angiotensin II in target tissues, the evidence for the presence of functional tissue RAS and the data that suggest a role for these tissue RAS in the pathophysiology of heart failure. Activation of circulating neurohormones is predictive of worsened survival in heart failure; however, cardiac and renal tissue RAS activities are also increased in the compensated stage of heart failure, when plasma renin-angiotensin activity is normal. It is hypothesized that the plasma RAS maintains circulatory homeostasis during acute cardiac decompensation, while changes in tissue RAS contribute to homeostatic responses during chronic sustained cardiac impairment. This concept of different functions of circulating and tissue RAS in the pathophysiology of heart failure may have important pharmacologic implications.
循环肾素-血管紧张素系统（RAS）在维持心血管稳态中起重要作用。最近有研究表明，内源性RAS存在于对心血管调节至关重要的靶组织中。本文综述了血管紧张素II在靶组织中的多种作用、功能性组织RAS存在的证据，以及提示这些组织RAS在心力衰竭病理生理学中发挥作用的数据。循环神经激素的激活预示着心力衰竭患者生存率恶化；然而，在心力衰竭代偿期，当血浆肾素-血管紧张素活性正常时，心脏和肾脏组织RAS活性也会增加。据推测，血浆RAS在急性心脏失代偿期间维持循环稳态，而组织RAS的变化则在慢性持续性心脏损伤期间促成稳态反应。循环和组织RAS在心力衰竭病理生理学中的不同功能这一概念可能具有重要的药理学意义。
