Oxidative Stress Biomarkers in Hypertension

Arterial hypertension is a silent and progressive disease with deleterious vascular implications on all target organs, including the heart, the brain, the kidneys, and the eyes. Oxidative stress, defined as the overproduction of Reactive Oxygen Species (ROS) over antioxidants, is capable of deteriorating not only the normal endothelial but also the cellular function with further cardiovascular implications. Xanthine oxidase activity, NADPH oxidase overexpression, and ROS production lead to hypertension and high arterial tone, culminating in end-organ damage. The inactivation of NO by superoxide reduces vasodilation and promotes peroxynitrite formation, which damages cellular components. Activation of MMPs by oxidative stress contributes to pathological neovascularization and angiogenesis. Salucin-β-induced activation of Angiotensin-II and NADPH results in vascular remodeling and fibrosis, while lipid peroxidation and PARP- 1 activation further exacerbate cellular apoptosis and vascular calcification. Moreover, to reliably assess the oxidative status an emerging number of biomarkers are under investigation. Antioxidant therapy, alongside traditional antihypertensive agents such as beta-blockers and ACE inhibitors, offers the potential to mitigate oxidative stress and its detrimental effects. Additionally, polyphenols, found in plant-based foods, show promise in managing oxidative stress in hypertensive patients although this data has not been confirmed in randomized clinical trials. Understanding the intricate relationship between oxidative stress and hypertension underscores the importance of developing comprehensive therapeutic strategies to reduce cardiovascular risk and improve patient outcomes.