Ramón Rodrigo

By Ramón Rodrigo, Roberto Brito and Jaime González

Experimental evidence supports a pathogenic role of free radicals or reactive oxygen species (ROS) in the mechanism of hypertension. Indeed, vascular ROS produced in a controlled manner are considered important physiological mediators, functioning as signaling molecules to maintain vascular integrity by regulating endothelial function and vascular contraction‐relaxation. However, oxidative stress can be involved in the occurrence of endothelial dysfunction and related vascular injury. Thus, ROS activity could trigger pathophysiological cascades leading to inflammation, monocyte migration, lipid peroxidation, and increased deposition of extracellular matrix in the vascular wall, among other events. In addition, impairment of the antioxidant capacity associates with blood pressure elevation, indicating potential role of antioxidants as therapeutic antihypertensive agents. Nevertheless, although increased ROS biomarkers have been reported in patients with essential hypertension, the involvement of oxidative stress as a causative factor of human essential hypertension remains to be established. The aim of this chapter is to provide a novel insight into the mechanism of essential hypertension, including a paradigm based on the role played by oxidative stress.

Part of the book: Update on Essential Hypertension

By Pablo Parra and Ramón Rodrigo

Acute myocardial infarction (AMI) is the leading cause of mortality worldwide. Major advances in the treatment have included coronary interventions, such as systemic thrombolysis and percutaneous coronary angioplasty (PCA). These procedures have been aimed to recover the blood flow in the cardiac zones affected by the occlusion of a branch of the coronary artery. However, damage is generated in the heart tissue known as myocardial reperfusion injury, an event associated with increased oxidative stress. Reactive oxygen species (ROS) are able to trigger cell death pathways, and myocardial structural and functional impairment. Studies on animal models of AMI suggest that lethal reperfusion accounts for up to 50% of the final size of a myocardial infarct, a part of the damage likely to be prevented. Although a number of strategies have been aimed to ameliorate lethal reperfusion injury, up to date the beneficial effects in clinical settings remain elusive. The accumulated body of evidence suggests that redox balance is a crucial determinant of ischemia–reperfusion injury, with clear mechanistic insights into pharmacological approaches. This chapter presents the molecular basis for a novel cardioprotection of patients with AMI subjected to PCA, based on a reinforcement of the antioxidant system.

Part of the book: Free Radicals and Diseases