Division of Endocrinology and Metabolism, Department of Medicine, University of Virginia Health System, P.O. Box 801414, Charlottesville, VA 22908, USA.
Pflugers Arch. 2013 Jan;465(1):99-110. doi: 10.1007/s00424-012-1146-3. Epub 2012 Sep 5.
The renin-angiotensin system (RAS) is a coordinated hormonal cascade intimately involved in cardiovascular and renal control and blood pressure regulation. Angiotensin II (Ang II), the major RAS effector peptide, binds two distinct receptors, the angiotensin type-1 receptor (AT(1)R) and the angiotensin type-2 (AT(2)R) receptor. The vast majority of the physiological actions of Ang II, almost all of them detrimental, are mediated by AT(1)Rs. In contrast, AT(2)Rs negatively modulate the actions of AT(1)Rs under the majority of circumstances and generally possess beneficial effects. AT(2)Rs induce vasodilation in both resistance and capacitance vessels, mediating natriuresis directly and via interactions with dopamine D1 receptors in the renal proximal tubule. AT(2)Rs inhibit renin biosynthesis and secretion and protect the kidneys from inflammation and ischemic injury. Our understanding of the exact role of AT(2)Rs in physiology and pathophysiology continues to expand; the purpose of this review is to provide an up-to-date summary of the functional role of AT(2)Rs at the organ, tissue, cellular, and subcellular levels with emphasis on the vascular and renal actions that bear on blood pressure regulation and hypertension.
肾素-血管紧张素系统（RAS）是一个协调的激素级联反应，与心血管和肾脏控制以及血压调节密切相关。血管紧张素 II（Ang II）是 RAS 的主要效应肽，它结合两种不同的受体，血管紧张素 1 型受体（AT(1)R）和血管紧张素 2 型（AT(2)R）受体。Ang II 的绝大多数生理作用，几乎都是有害的，都是通过 AT(1)Rs 介导的。相比之下，AT(2)Rs 在大多数情况下负向调节 AT(1)Rs 的作用，通常具有有益的效果。AT(2)Rs 可引起阻力和容量血管的扩张，通过与肾近端小管中的多巴胺 D1 受体相互作用直接介导利钠作用。AT(2)Rs 抑制肾素的生物合成和分泌，并保护肾脏免受炎症和缺血性损伤。我们对 AT(2)Rs 在生理学和病理生理学中的确切作用的理解仍在不断扩展；本文的目的是提供一份最新的综述，总结 AT(2)Rs 在器官、组织、细胞和亚细胞水平的功能作用，重点介绍与血压调节和高血压有关的血管和肾脏作用。
