The Immune System, Nahmod et al. (1972) first demonstrated that angiotensin degranulaba the mast-cell serotonin released into the environment, this amine also have pressor effects increased synthesis and was released by angiotensin II in the central nervous system, and second that the AII caused an increase leukocyte migration and inhibited the MIF (factor inhibiting the migration) where Ca + dependiente.Sin this phenomenon, however, this was not sufficient to understand the disease called hypertension, for the greatest achievements occurred in the past 25 years to first synthesized inhibitors and then converting enzyme receptor blockers, angiotensin AT-1 and AT-2. While Inagami in 1981 first described the localization of angiotensin II in kidney mesangial cells, it was not until 1992 when Nahmod et al. discover that angiotensin I and II is at the level of circulating cells, mononuclear phagocytic system, preferably when activated by different stimuli (LPS, cholesterol, immune complexes, etc.) and angiotensin of mononuclear cells in either intracrina way or acting in angiotensin autoreceptor regulates the production of TNF-alpha and other cytokines that have a pro-inflammatory activity .. The T lymphocyte is directly activated by angiotensin II causing an increased synthesis and release of interferon gamma (IF-gamma) Moreover, these same activators (LPS or infectious processes) increase the expression of angiotensin II receptor level membrane amplifying cell polypeptide deleterious response. A few years earlier (1986) the same group first discovered that both angiotensin II and saline expansion la liberation and increased production of an inhibitor of the enzyme activated membrane ATPase by sodium and potassium (Na-K-ATPase) is that a substance similar to ouabain (demonstrated, which was an endogenous ouabain) and that this effect was blocked by the angiotensin II analogue applied through intra-cerebro-ventricular, the saralasina.