Arterial hypertension represents a major cardiovascular epidemic condition,
with a prevalence of more than 25% throughout the adult population, affecting nearly
one billion individuals around the globe. It remains asymptomatic until later in its
course, but as a long-term consequence of this condition, accumulating damage in
specific organs propagates the development of cardiac pathologies, renal failure,
cerebrovascular pathologies and vascular dementia, atherosclerotic vascular disease
and retinopathy. Several processes are involved in these pathogenic alterations
including endothelial activation, growth and migration of vascular smooth muscle cells,
expression of pro-inflammatory mediators, changes in collagen turnover and the
remodeling of extracellular matrix. Complex biochemical, hormonal and
hemodynamic mechanisms form the basis of these alterations, referred as
hypertensive target organ damage, however, the common ground is the excess
generation of reactive oxygen species/ROS2, which, in addition to governing these
pathological changes, possesses direct damaging properties6. Additional factors
accompanying chronic hypertension may amplify these processes, including arterial
stiffness, effects of sympathetic over-activity, dysregulation of tissue perfusion and
increased activity of several hormone systems, especially the renin-angiotensinaldosterone
system/RAAS2