Angiotensin II induced cerebral microvascular inflammation and increased blood–brain barrier permeability via oxidative stress

Abstract Although hypertension has been implicated in the pathogenesis of vascular disease, its role in inflammatory responses, especially in brain, remains unclear. In this study we found key mechanisms by which angiotensin II (AngII) mediates cerebral microvascular inflammation. C57BL/6 male mice were subjected to slow-pressor dose of AngII infusion using osmotic mini-pumps at a rate of 400 ng/kg/min for 14 days. Vascular inflammation in the brain was evaluated by analysis of leukocyte–endothelial interaction and blood–brain barrier (BBB) permeability. Results from intravital microscopy of pial vessels in vivo , revealed a 4.2 fold ( P