Inflammation is a key feature in the initiation, progression, and clinical implications of cardiovascular disorders, including essential hypertension. Increasing evidence shows that activation of renin-angiotensin-aldosterone system and enhanced local production of angiotensin II have been implicated in the pathophysiology of inflammation.
Besides being a potent vasoactive peptide, angiotensin II regulates the inflammatory process. Specifically, it increases vascular permeability, participates in the recruitment of inflammatory cells and their adhesion to the activated endothelium, and regulates cell growth and fibrosis. Reactive oxygen species are implicated at every stage in inflammation and activate multiple intracellular signaling molecules and transcription factors associated with inflammatory responses, such as nuclear factor-kappa B and activator protein-1. Other components of the renin-angiotensin-aldosterone system, including aldosterone and/or mineralocorticoid receptor, induce the production of reactive oxygen species and participate in vascular inflammation. Several studies suggest a role of endothelin-1 as an important mediator of chronic inflammation and there is an increasing interest in the relationship between endothelin-1 and reactive oxygen species. These data may have great impact on future therapeutic strategies.