Acute renal failure (ARF) is a clinical syndrome characterized by deterioration of renal function. The principal causes of ARF are ischemic and toxic insults that can induce tissue hypoxia. Transcriptional responses to hypoxia can be inflammatory or adaptive with the participation of the hypoxia-inducible factor 1 (HIF-1), and the expression of specific genes related to oxidative stress. The production of peroxynitrites, and protein nitrotyrosylation are sequelae of oxidative stress. Inflammatory responses have been related to COX-2 suggesting that its activation might play an important role in the pathogenesis and progression of nephropathies such as ARF. In the kidney, renin and bradykinin participate on the regulation of COX-2 synthesis. With the hypothesis that in ARF there is an increase in the expression of agents involved in adaptive and inflammatory responses, the distribution pattern and abundance of COX-2, its regulators renin, kallikrein, bradykinin B2 receptor and oxidative stress elements, heme oxygenase-1(HO-1), erythropoietin (EPO), inducible nitric oxide synthase (iNOS) and nitrotyrosylated residues were studied by immunohistochemistry and immunoblot analysis in rat kidneys after bilateral ischemia. In kidneys with ARF an important initial damage was demonstrated by PAS staining and by the induction of the damage markers -SMA and ED-1. Coincidently with the major damage, an increase in the abundance of EPO, HO-1, iNOS, renin and bradykinin B2 receptor was observed. In spite of the B2 receptor induction, we observed an important decrease in COX-2 in the ischemic/reperfused kidney. These results suggest that COX-2 does not participate in inflammatory responses induced by hypoxia.