Conversely, in a rat model of CHF, intravenous administration of adenovirus carrying EcSOD, not EcSOD with deleted HBD or R213G mutation, resulted in increased EcSOD binding to endothelium and increased SOD activity in the aorta, reduced levels of superoxide and peroxinitrite, and improved relaxation to acetylcholine and ADP in the aorta and mesenteric artery [51]. This evidence concerns the gene SOD3 and congestive heart failure.