Since arginase-I and NOS2 compete for the same substrate, arginine, we developed a tissue-specific arginase-I deficient mouse model [76], to determine whether the absence of arginase-I in endothelial cells and macrophages would exhibit beneficial effects on the arginine concentration and NO production during endotoxemia [76]. This evidence concerns the gene NOS2 and serum lipopolysaccharide activity.