Cardiovascular diseases are a leading cause of mortality and morbidity worldwide, with hypertension being a major risk factor. Numerous studies support the contribution of reactive oxygen and nitrogen species in the pathogenesis of hypertension, as well as other pathologies associated with ischemia/reperfusion. However, the validation of oxidative stress-related biomarkers in these settings is still lacking and novel association of these biomarkers and other biomarkers such as endothelial progenitor cells, endothelial microparticles, and ischemia modified albumin, is just emerging. Oxidative stress has been suggested as a pathogenic factor and therapeutic target in early stages of essential hypertension. Systolic and diastolic blood pressure correlated positively with plasma F2-isoprostane levels and negatively with total antioxidant capacity of plasma in hypertensive and normotensive patients. Cardiac surgery with extracorporeal circulation causes an ischemia/reperfusion event associated with increased lipid peroxidation and protein carbonylation, two biomarkers associated with oxidative damage of cardiac tissue. An enhancement of the antioxidant defense system should contribute to ameliorating functional and structural abnormalities derived from this metabolic impairment. However, data have to be validated with the analysis of the appropriate oxidative stress and/or nitrosative stress biomarkers. 1. Introduction Cardiovascular diseases are a leading cause of mortality and morbidity worldwide [1], with hypertension being a major risk factor [2]. These diseases affect more than 600 million people and it is estimated that there will be 29% of the world adult population suffering hypertension by 2025 [3]. The pathophysiology of cardiovascular diseases is complex due to the multiple biological pathways that have been implicated. Accordingly, the absolute risk of future cardiovascular events cannot be estimated from a single biomarker. These diseases are originated in the vascular endothelium, a target for the classical cardiovascular risk factors. Following endothelial activation oxidative stress has an important role in the development of atherosclerosis [4] and hypertension [5, 6], thereby contributing to the progression of the structural and functional cardiovascular damage. In cardiovascular disease related to ischemia/reperfusion injury, redox imbalance triggers the activity of a number of signaling pathways mediated by reactive oxygen species (ROSs) and reactive nitrogen species (RNSs) [7]. Consequently, in cardiac surgery with extracorporeal
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