SOD1 and endothelial dysfunction: Likewise, coronary resistance vessels from apoE-/- mice demonstrate a preserved function of the PGI2 system; however, NADPH induced •O2- formation was enhanced in cardiac extracts from hearts, and the vasodilator response to bradykinin was practically abolished by an SOD mimetic [105] indicating that the endothelial dysfunction in these vessels is likely mediated by the inactivation of bioavailable NO by •O2-.