Antioxidants in Hypertension

Millions of people worldwide suffer from hypertension, which is a significant risk factor for cardiovascular disease. Hypertension is responsible for various dysfunctions, including major organ tissue damage through oxidative mechanisms, lipid peroxidation, and myocardial dysfunction resulting from impairment in microvascular function. Oxidative stress, a powerful imbalance between the body's antioxidant defenses and the production of reactive oxygen species (ROS) and nitrogen species (RNS), is significant evidence of its complex pathogenesis. An abundance of ROS/RNS as destructive substances affects blood vessels through critical components such as endothelial cells and nitric oxide (NO) bioavailability, which ultimately leads to vascular dysfunction and hypertension. Apart from the endothelial cells and reduced NO, oxidative stress is also caused by redox signaling, insufficient antioxidants, and the neurohumoral system. Examining the complex interaction between antioxidants and hypertension, many studies explores how they may impact the onset of the disease and current and possible treatment approaches. On the other hand, endogenous antioxidants, which include substances like glutathione, catalase, and superoxide dismutase (SOD), function as cellular defenders and free radical scavengers, reducing the detrimental effects of ROS/RNS. Antioxidants play a significant role in the standardization process by lowering levels of superoxide, hydrogen peroxides, and organic hydroperoxides. In human and animal research, antioxidant treatment of hypertension has been found to lower blood pressure and enhance vascular function. Antioxidants may affect hypertension through various processes, inflammatory pathway modulations, neurohumoral regulation, endothelial repair, improved vascular tone, and rising blood pressure. Personalized antioxidant therapy is being made possible by recent research exploring the possibility of certain antioxidants focusing on certain ROS species, assembly of NADPH oxidase, signaling pathways (AMPK, TyrRS-PARP1, SIRT3, MAPK, TLR4, etc.), arterial stiffness, B and T cell proliferation, and activation of enzymes (nitric oxide synthase and Nrf2). More contemporary techniques, such as atrial natriuretic peptide (ANP) to block angiotensin II (Ang-II) and an antioxidant microinjection into the rostral ventrolateral medulla (RVLM) to directly shift ROS to NO, have been used to influence neurohumoral activity and manage hypertension. Many antioxidants under clinical trials have great potential for managing hypertension, although there are still barriers to overcome. The review urges more investigation into the complexities of the antioxidant-hypertension axis to develop therapeutic strategies to fully utilize antioxidants in the fight against hypertension.