ROS are released upon the activation of phagocytic NOS by acute myocardial infarction or reperfusion injury whereas abnormal stimulation of nonphagocytic NOS by angiotensin II, catecholamines and TNF-α has been implicated in cardiac hypertrophy collagen deposition, metalloprotease activation, fibrosis and heart failure [69]. This evidence concerns the gene AGT and cardiac hypertrophy.