Inflammatory cell infiltration plays a key role in the onset and progression of renal injury. The NF-κB participates in the inflammatory response, regulating many proinflammatory genes. Angiotensin II (Ang II), via AT1 and AT2 receptors, activates NF-κB. Although the contribution of Ang II to kidney damage progression is already established, the receptor subtype involved in the inflammatory cell recruitment is not clear. For investigating this issue, the unilateral ureteral obstruction (UUO) model was used in mice, blocking Ang II production/receptors and NF-κB pathway. Two days after UUO, obstructed kidneys of wild-type mice presented a marked interstitial inflammatory cell infiltration and increased NF-κB activity. Treatment with AT1 or AT2 antagonists partially decreased NF-κB activation, whereas only the AT2 blockade diminished monocyte infiltration. Obstructed kidneys of AT1-knockout mice showed interstitial monocyte infiltration and NF-κB activation; both processes were abolished by an AT2 antagonist, suggesting AT2/NF-κB involvement in monocyte recruitment. In wild-type mice, only angiotensin-converting enzyme inhibition or combined therapy with AT1 plus AT2 antagonists blocked monocyte infiltration, NF-κB activation, and upregulation of NF-κB–related proinflammatory genes. Therefore, AT1 and AT2 blockade is necessary to arrest completely the inflammatory process. Treatment with two different NF-κB inhibitors, pirrolidin-dithiocarbamate and parthenolide, diminished monocyte infiltration and gene overexpression. These data show that Ang II, via AT1 and AT2 receptors and NF-κB pathway, participates in the regulation of renal monocyte recruitment and may provide a rationale to investigate further the role of AT2 in human kidney diseases.