This result argues for the contribution of increased vascular arginase activity to NO deficiency in AIA rats, and demonstrated that in vivo arginase inhibition restores the equilibrium between NOS and arginase pathways, as previously identified in animal models of cardiovascular diseases, such as hypertension [10,11], atherosclerosis [13] or ageing [14]. The gene discussed is NOS2; the disease is atherosclerosis.