Immune mechanisms in angiotensin II-induced target-organ damage

Inflammation and activation of immunity are central features in the pathogenesis of atherosclerosis, ischemic myocardial injury, and hypertension-induced target-organ damage. The renin-angiotensin-aldosterone system can initiate not only innate but also acquired immunity. The latter process includes formation of activating antibodies directed at the angiotensin (Ang) II receptor. Ang II not only regulates vascular tone and sodium balance, but also activates immune cells and promotes cell infiltration into target organs. Studies showed that macrophages and various T cell subtypes play a pivotal role in target-organ damage and even in the regulation of blood pressure and responses to Ang II. Experimental and clinical evidence shows that adaptive transfer of immune cells, rendering mice deficient for a certain subset of immune cells, or immunosuppressive treatment affects blood pressure and ameliorates target-organ damage. Neural mechanisms interact with and regulate these processes. Understanding the mechanisms could direct us to novel therapies.