The angiotensin AT2 receptor in inflammation

Chronic inflammation is increasingly regarded not just as a consequence of a continuous infectious hazard, but also as an integral part of many noninfectious diseases such as autoimmune disorders, diabetes or cardiovascular disease. Thus, it is not surprising that some hormonal systems, like the renin-angiotensin system (RAS), which were originally described in the context of cardiovascular disease have also turned out to be major regulators of the inflammatory response. This review focuses on the role of the RAS in inflammation, with particular emphasis on the role of the angiotensin AT(2) receptor. While the proinflammatory features of the angiotensin AT(1) receptor are well established, most current evidence supports an anti-inflammatory role for AT(2) receptor. However, data on this receptor in inflammation are still rather sparse and are somewhat controversial. This article will discuss the principal mechanisms of AT(2) receptor-coupled interference with proinflammatory pathways as well as data derived from animal models of specific diseases. Finally, it will give a brief outlook into new possibilities in AT(2) receptor research and in the potential utilization of AT(2) receptor stimulation as a novel pharmacological concept in anti-inflammation.