**5. Angiotensin II: role in immunosenesence**

AT II is considered to stimulate the production of molecular oxygen species that trigger mitochondrial dysfunction and cellular injury [21]. AT II via AT1R stimulation has been shown to activate NAD(P)H oxidase to produce ROS, resulting in oxidative stress damage [21]. It has been proposed that ROSs are the most prominent molecular species involved in the aging process [22]. ROSs have been revealed to contribute significantly to various age-associated organ failures, including hypertension, cardiovascular diseases, and renal damage [22]. Hence, AT II is considered to be involved in organ senescence related to its ability to mediate the release of oxidant species [23]. Recent studies have disclosed that AT II-induced ROS production leads to functional and structural changes of blood vessels that result in vascular senescence and age-related vascular diseases [23]. Previous studies related to the long-term effects of AT II inhibition by either ACEi or ARBs disclosed protective effects on the cardiovascular system of rats and revealed the prolongation of the life span of rats [24, 25]. Another study disclosed that old mice lacking AT1R did not develop age-related cerebral circulation damage caused by the accumulation of oxygen radicals [26]. The inhibition of RAS has been disclosed to reverse age-related advanced myocardiac hypertrophy and fibrosis in old hypertensive rats, and the protective effect presumably was considered to involve the suppression of AT II-mediated oxidative stress, as disclosed by reduced expression of NAD(P)H oxidative components in the hearts of aged rats [26].
