The aim of this review is to comment the results described in the literature concerning the possible pharmacodynamic mechanisms involved in the improvement of quality of life of angiotensin converting enzyme inhibitors that is just a working hypothesis. These drugs, widely used in the treatment of hypertension, prevent the formation of angiotensin II and the generation of free radicals, as well as the hydrolysis of bradykinin, enkephalins and endorphins. Different mechanisms have been implicated on quality of life: 1) increase of bradykinin levels in the central nervous system that would trigger the release of nitric oxide (NO), noradrenaline, acetylcholine, excitatory amino acids and vasopressin which are involved in memory and cognition; 2) increase of brain blood supply by enhanced NO synthesis; 3) interference with cholinergic mechanisms in the central nervous system by angiotensin II inhibition of acetylcholine release; 4) decrease of endorphin metabolism; and 5) interaction with hypothalamic-pituitary-adrenal axis that releases ACTH and vasopressin.