To examine whether decreased activation of endothelial nitric oxide synthase (eNOS) has a role in the Tat-induced endothelial dysfunction, aortic rings from control and chronic Tat-treated mice were pretreated with NOS-inhibitor N (ω)-nitro-L-arginine methyl ester (L-NAME) followed by measurements of relaxation responses to ACh. This evidence concerns the gene NOS3 and endothelial dysfunction.