Oxidative Stress, Antioxidants and Hypertension

Figures

• 

  Figure 1. Impact of physiological and pathophysiological stimuli on the regulation of vascular and cardiac function and cardiovascular diseases. Physiological stimuli like exercise can induce redox-sensitive signal transduction and the regulation of vascular and cardiac function. Redox-sensitive signal transduction, gene and protein expression and the regulation of vascular and cardiac function are also present in patients with cardiovascular diseases, despite being altered. Clinical risk factors and the metabolic syndrome can increase levels of vasoactive substances like angiotensin II, oxidative stress, cell and tissue damage, as well as in long-term cardiovascular diseases. Created with BioRender.com.

• 

  Figure 2. Physiological redox balance and oxidative stress. Under physiological conditions, the production of reactive oxygen species (ROS) and the antioxidative capacity are in a balance. An increased production of ROS, e.g., by NADPH oxidase (NOX) isoforms 1, 2 and 5, which is not compensated by antioxidative defense mechanisms like the different superoxide dismutase (SOD) isoforms, can lead to oxidative stress. Created with BioRender.com.

• 

  Figure 3. ROS formation and hypertension. Activation of NADPH oxidases (NOX) and other sources of reactive oxygen species (ROS) promotes oxidative stress, and leads to organ damage, vascular dysfunction and hypertension. Parts of figure are adapted from SMART—Servier Medical Art, Servier: https://smart.servier.com. https://creativecommons.org/licenses/by/3.0/ (accessed on 22 September 2022).