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Transactivation of growth factor receptors (GFRs) by angiotensin II (Ang II) and endothelin-1 (ET-1), through their G protein–coupled receptors (GPCRs), stimulate NADPH oxidase (Nox)–derived reactive oxygen species (ROS) production and activation of ROS-signalling pathways that influence cardiovascular processes leading to hypertension-associated target-organ damage.
