Thus, the pathophysiology of AH involves changes in its different mechanisms (baroreflex dysfunction, increased sympathetic activation, alterations in the renin-angiotensin-aldosterone system, increased NAD(P)H oxidase activity, oxidative stress, and endothelial dysfunction) [7], whose common trait is endothelial dysfunction, characterized by the low availability of nitric oxide (NO) and the consequent local imbalance between factors of relaxation and constriction of arterioles [8]. Here, REN is linked to endothelial dysfunction.