Figure 5.

NADPH oxidase-derived ROS in renovascular hypetertension. Activation of PKC, Rac1, and tyrosine kinase receptors increases ROS production via activation of NADPH oxidase. ROS-induced inhibition of endothelium-dependent vasodilatation can be abrogated by inhibition of PKC, Rac, and EGFR kinase in renovascular animal model (using clipped WT mice), suggesting that activation of NADPH oxidase-derived ROS plays a crucial role in the development of renovascular hypertension. PEG-SOD: Polyethylene glycol-conjugated superoxide dismutase; WT: Wild type.