Microvascular changes in the brain are significant causes of cerebral edema and ischemia injury. A number of studies suggest that angiotensin (Ang) Ⅱ may be involved in the initiation and regulation of processes occurring in brain ischemia. We recently reported that Ang Ⅱ injures brain microvascular endothelial cells (BMEC) partially via stimulating intercellular adhesion molecule-1 (ICAM-1) expression. However, the signaling cascade leading to Ang Ⅱ-induced ICAM-1 expression in BMEC was unclear. The present study tested the hypothesis that Ang Ⅱ induces ICAM-1 expression via an AT1 receptor/nuclear factor-кB (NF-кB) pathway in BMEC. Ang Ⅱ directly stimulated the expression of ICAM-1 mRNA and protein in primary cultured BMEC. Ang Ⅱ treatment also resulted in the degradation of InBa and increase of NF-кB p65 subunit in the nucleus as well as the DNA binding activity of nuclear NF-кB. These effects were abolished by pretreatment with the selective AT1 receptor antagonists, losartan and compound EXP-2528, or losartan plus the AT2 receptor antagonist PD123319, but not by PD123319 alone. Moreover, there were no significant differences between the losartan and losartan plus PD123319 groups. These findings indicate that Ang ⅡⅡ-induced ICAM-1 upregulation in brain microvascular endothelial cells may be mediated via an AT1 receptor/NF-nB pathway.