[The renin saga].

This saga is the story of a scientific development. From the search of a mechanism to explain high blood pressure, research was orientated to the functions of an omnipresent biochemical system. And from the search to elucidate the etiology of arterial hypertension, research has ended up studying the local, functional and structural activity of the renin-angiotensin system and the possibilities of interfering with its actions. Since Bright, left ventricular hypertrophy became associated with nephrosclerosis. Later on, clinical studies led Volhard and Fahr to associate nephrosclerosis to high blood pressure while biochemical research led Tigerstedt and Bergmann to demonstrate that renin was associated to high blood pressure. Two teams of investigators, one in Argentina and one in USA discovered the biochemical mechanism by which renin acted on arterioles and later on, two other teams, one in USA and one in England, discovered the biochemical steps leading to the synthesis of angiotensin II. Since Goldblatt's experimental design resulting in a reliable method to obtain arterial hypertension, more than 20 years had to elapse before renal artery stenosis became established as the main cause of clinical secondary arterial hypertension. The renin-angiotensin system became part of a very complex array of substances able to regulate local circulation directly or indirectly and angiotensin has become involved in the remodeling of the smooth muscles of arterioles and myocardium.