Role of the renin–angiotensin system in vascular inflammation

Angiotensin (Ang) II, the main effector of the renin–angiotensin system (RAS), is one of the major mediators of vascular remodeling in hypertension. Besides being a potent vasoactive peptide, Ang II exerts proinflammatory effects on the vasculature by inducing integrins, adhesion molecules, cytokines and growth and profibrotic mediators through activation of redox-sensitive pathways and transcription factors. Clinical findings suggest that inflammation participates in the mechanisms involved in the pathophysiology of hypertension and its complications. Antagonists of the RAS have been shown to exert cardiovascular protection, in part through their vascular anti-inflammatory effects. However, further studies are needed to better understand whether inflammatory biomarkers might be clinically useful for cardiovascular risk stratification and whether targeting inflammation pharmacologically will improve cardiovascular outcomes beyond blood pressure reduction. The present review addresses recent findings regarding the pathophysiology of vascular inflammation in hypertension, focusing specifically on the role of Ang II.