FIG. 6.
Angiotensin II-induced ROS production via NADPH oxidase. AngII binds to its receptor (AT1R) and induces PKC via the Gq-PLC pathway—which is dependent on DAG as well as on increased cytosolic Ca2+ ions. PKC then activates Nox, blocks Cl− influx, and induces the K+ export. Nox produces superoxide anions (O2·), which open mitochondrial ATP-dependent potassium channels (mitoKATP). This, subsequently, leads to increased mitochondrial ROS production, which gets released in the cytosol. The increasing amount of ROS further induces PKC and the Ca2+ influx and blocks Cl− import. ROS is associated with catabolic mechanism, such as apoptosis, autophagy, and protein degradation. DAG, diacylglycerol; Nox, NADPH oxidase; PKC, proteinkinase C; PLC, phospholipase C. To see this illustration in color, the reader is referred to the web version of this article at www.liebertpub.com/ars