Key result
High concentrations or prolonged exposure to angiotensin II and aldosterone activate NADPH oxidase, generating reactive oxygen species that induce signaling processes and DNA damage.
This review highlights how high concentrations of blood pressure-regulating hormones angiotensin II and aldosterone induce reactive oxygen species generation, leading to altered cellular signaling and DNA damage.
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May drive oxidative DNA damage in hypertension; hypothesis-generating for antioxidant adjuncts to RAAS blockade.
The formation of reactive oxygen species (ROS) can be induced by xenobiotic substances, such as redox cycling molecules, but also by endogenous substances such as hormones and cytokines. Recent research shows the importance of ROS in cellular signaling. Here, the signaling pathways of the two blood pressure-regulating hormones angiotensin II and aldosterone are presented, focusing on both their physiological effects and the change of signaling owing to the action of increased concentrations or prolonged exposure. When present in high concentrations, both angiotensin II and aldosterone, as various other endogenous substances, activate NADPH oxidase, which produces superoxide. In this review the generation of superoxide anions and hydrogen peroxide in cells stimulated with angiotensin II or aldosterone, as well as the subsequently induced signaling processes and DNA damage is discussed.
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Queisser et al. (2010) conducted a review in Reactive oxygen species generation in angiotensin II and aldosterone signaling. Angiotensin II and aldosterone was evaluated on Generation of superoxide anions and hydrogen peroxide, signaling processes, and DNA damage. High concentrations or prolonged exposure to angiotensin II and aldosterone activate NADPH oxidase, generating reactive oxygen species that induce signaling processes and DNA damage.
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