In addition, B2 receptor activation activates endothelial nitric oxide synthase (eNOS) and simulates the release of nitric oxide (NO), prostacyclin, and kinins to inhibit vascular smooth muscle growth and neointima formation, which may inhibit atherosclerosis development; conversely, B1 receptor activation, results in a prolonged high output of NO by inducible nitric oxide synthase (iNOS) and may have deleterious effects [6]. This evidence concerns the gene NOS2 and atherosclerosis.