La angiotensina II y la inflamación: El efecto de la inhibición de la ECA y del bloqueo del receptor de angiotensina II

It has recently been shown that angiotensin II (Ang II) exerts a pro-inflammatory effect on leucocytes, endothelial cells and vascular smooth muscle cells. This review discusses the effect of Ang II on inflammation and oxidative stress and the anti-inflammatory effects of ACE inhibitors and Ang II receptor blockers (ARBs). Ang II, acting via at type1 receptor, activates nuclear factor kappa B (NF-kB, an inflammatory transcription factor) mediated transcription and gene expression and increases adhesion molecules and chemokines, thereby predisposing to a pro-thrombotic state as well as plaque rupture. Ang II also stimulates NADPH oxidase and enhances ROS production. This decreases nitric oxide bioavailability and causes endothelial dysfunction. Valsartan suppresses ROS (O₂^.) generation by leucocytes and intranuclear NF-kB binding activity; it increases inhibitory kappa B (IkB) expression while decreasing plasma CRP concentrations. It is likely that this action of ARBs contributes to their beneficial effects on cardiovascular events in clinical outcome studies.