EDN1 and endothelial dysfunction: Furthermore, IPC can attenuate or eliminate O2− production and its effects by suppressing endothelin-1 (ET-1) secretion via the opening of these mitochondrial KATP channels prior to subsequent ischemic events, since ET-1 generation is related to increased production of superoxide anion and endothelial dysfunction with increased P-selectin expression and neutrophil adhesion [130].