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.