In healthy conditions, the endothelium plays a pivotal role in maintaining vascular homeostasis, mainly by the production of the relaxing factor nitric oxide (NO), which protects the vessel wall from those mechanisms favouring the development of vascular atherosclerosis. Aging is a powerful cardiovascular risk factors associated with endothelial dysfunction. In details, an alteration in the NO substrate L-arginine is the major factor responsible for endothelial dysfunction with advancing age, while reactive oxygen species (ROS) excess generation, which in turn reduce NO availability, plays a role in oldest individuals only. NO inhibition by ROS excess is the main cause of endothelial dysfunction which occurs in many other clinical conditions including arterial hypertension. Although hypertension induces early vascular aging in several arterial districts, however vascular features of physiological aging and hypertension are not necessarily similar. While an impaired NO availability represents the common final effect, aging and hypertension seem to adopt different mechanisms, at least at the level of microcirculation. Indeed, physiological aging shows a progressive reduced NO availability, while in advanced age some degree of oxidative stress emerges. In hypertensive patients, NO availability is early reduced, but the progression rate with age appears to be similar. Whether the hypertensive- and age-related vascular alterations represent only a mere additive effect of two independent risk factors resulting in endothelial dysfunction awaits further clarification.
Keywords: Ageing; Endothelial function; Microcirculation; Nitric oxide; Oxidative stress.