In 1952, Skeggs recognizes two forms of angiotensin, the first a decapeptide called angiotensin I and degradation by a converting enzyme (kininase II) formed an octapeptide called angiotensin II. In 1957, Ciba Laboratories, Schwyzer made polypeptide synthesis and Gross suggested that the renin-angiotensin system was involved in the regulation of aldosterone and observed that very small amounts of synthetic polypeptide or hyponatremia increases circulating renin in humans stimulated aldosterone secretion. However, he never demonstrated that plasma renin levels were correlated with levels of blood pressure in essential hypertension. Only in the late 1960s with the discovery by a team of researchers at the University ofBuenos Aires, Nahmod et al. They describe the polypeptide angiotensin I and II occurs at plasma and glomerular no requirement that this is synthesized at tissue level (Nature, 1969, FEBS 1970) luegoa finding that synthesis in many tissues such as brain, endocrine glands, blood vessels , immune system and primarily in cardiac tissue, which in addition to continuously synthesize in-vitro was the organ containing the highest concentration of the polypeptide. Nahmod et al., 1975 for the first time demonstrated by immunofluorescence that the peptide is distributed in discrete areas of the Nervous System Central, located in nuclei of the hypothalamic region circumventriculares areas that are involved in regulating blood pressure, water intake and sodium on the release of hypothalamic factors that control the release of neuro-pituitary hormones, also focusing on limbic area in the amygdala and the brainstem (nuclei of these that are related to behavior and the regulation of blood pressure).