NOS3 and endothelial dysfunction: The ROS-induced ROS production concept can be extended to almost any kind of source of RONS as almost all of these sources contain “redox switches.” For hypertension, it has been repeatedly shown that genetic deficiency in NADPH oxidase subunits, especially knockout of the phagocytic isoform NOX2 eliminating the superoxide formation from phagocytes, prevents eNOS uncoupling and endothelial dysfunction [129].