In 1939, two independent teams, in Buenos Aires and Indianapolis, identified the polypeptide angiotensin. In 1934, Goldblatt et al. demonstrated that partial occlusion of the renal arteries produces hypertension in dogs, and Houssay in 1936 predicted the presence of a humoral mechanism and, with Fasciolo, demonstrated that the ischemic kidneys released a pressor substance that increased the recipient's blood pressure. Later on, Taquini proved that the rise in blood pressure that follows the re-establishment of circulation in kidneys was also produced by a plasmatic substance from the venous blood of acute ischemic kidneys and it was called ‘hypertensin’. Then, they proved that it was the result of an enzymatic reaction in which renin was the enzyme and plasma the substrate. At the same time, in 1939, Page et al. postulated that renin activated by plasma becomes vasoactive and the substance was called ‘angiotonin’. Page's group began in 1937, with the purification of renin, studying its renal hemodynamic effects. Later on, Page et al. acknowledged in 1943 the enzymatic nature of the system and renamed their so-called renin-activator as renin substrate. Both groups fused the two original names into ‘angiotensin’ during a meeting at Michigan in 1958, making the ‘adventure of the discovery of angiotensin’ a reality.