ABSTRACT
Cardiovascular disease remains the leading cause of death worldwide, despite the great work that has taken place in preventing and controlling cardiovascular risk factors. In turn, hypertension is considered to be the most important risk factor in the development of cardiovascular disease (Yusuf et al. 2004). In recent years, oxidative stress (OS) has gained attention as one of the key mechanisms responsible for the development of cardiovascular morbidities. Although low levels of reactive oxygen species (ROS) could exert an important role in the homeostasis of the vascular wall, excessive ROS contribute to impaired endothelium-dependent dilation in part by decreasing nitric oxide (NO) bioavailability, a pathophysiological condition that leads to hypertension.
