The NO-cGMP pathway participates in vascular adaptation to oxidative stress in Nrf2 KO mice

Background Endothelial dysfunction is considered both as cause and consequence of oxidative stress. Mice lacking the transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2 KO) can be considered as a model of chronic adaption of the organism to oxidative stress, as they miss a key master switch controlling the expression of antioxidant and protective enzymes involved in the regulation of the cellular redox state. In this study we aimed to investigate the coronary and vascular phenotype and systemic hemodynamics of these mice compared to wild type (WT) littermates.