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The renin-angiotensin-aldosterone system (RAAS) through its physiological effectors plays a key role in promoting and maintaining inflammation. Inflammation is an important mechanism in the development and progression of cardiovoascular diseases (CVD) such as hypertension and atherosclerosis. In addition to its main role in regulating blood pressure and therefore its role in hypertension, RAAS has pro-inflammatory and profibrotic effects at cellular and molecular levels. Blocking RAAS provides beneficial effects for the treatment of cardiovascular and renal diseases. Evidence shows that inhibition of RAAS positively influences vascular remodeling thus improving vascular disease outcomes. The beneficial vascular effects of RAAS inhibition are likely due to decreasing vascular inflammation, oxidative stress, endothelial dysfunction, and positive effects on regeneration of endothelial progenitor cells (EPC). Inflammatory factors such as vascular cell adhesion molecule-1 (ICAM-1), tumor necrosis factor-α (TNFα), interleukin-6 (IL-6), and C-reactive protein (CRP) have key roles in mediating vascular inflammation, and blocking RAAS negatively modulates the levels of these inflammatory molecules. Some of these inflammatory markers are clinically associated with cardiovascular disease events. More studies are required to establish longterm effects of RAAS inhibition on vascular inflammation, vascular cells regeneration, and cardiovascular disease clinical outcomes. This review presents important information on RAAS’s role on vascular inflammation, vascular cells responses to RAAS effectors, and on inhibition of RAAS signaling in the context of vascular inflammation, vascular remodeling, and vascular inflammation-associated CVD. Nevertheless, the review also equates the need to re-think and rediscover new RAAS inhibitors.

The Rennin-Angiotensin-Aldosterone System (RAAS) in Vascular Inflammation and Remodeling