Introduction Arterial hypertension (AH) is one of the main modifiable risk factors for cardiovascular diseases, as it causes increased arterial stiffness and endothelial dysfunction since early stages. Sympathetic hyperactivity and activation of the renin-angiotensin-aldosterone system (RAAS) are among the major pathophysiological mechanisms of AH, in addition to an overproduction of reactive oxygen species (ROS) and imbalances in the nitric oxide (NO) availability. The increase in endothelial permeability in response to low NO synthesis explains the correlation of AH with atherosclerosis […]