The pathogenesis of chronic renovascular hypertension.

THE ROLE of the kidney in the regulation of arterial pressure was recognized as early as 1898 when Tigerstedt and Bergman demonstrated that kidney extracts possess a pressor action and gave the name renin to the substance producing the action. In 1934. Goldblatt and co-workers' produced chronic renal hypertension in dogs by renal artery constriction. This discovery was a major breakthrough because it provided an easy and reliable method to produce a model of human renovascular hypertension. Almost immediately, investigators began to search for a humoral mechanism to explain the pathogenesis of experimental renal hypertension. This search culminated in the discovery of the renin-angiotensin system in 1939 almost simultaneously by Page and Helmer in the United States and by Braun-Menendez and collaborators in Argentina. For four decades the complicated problem of renal hypertension has been investigated in attempts to define the pathogenic mechanisms, and much emphasis has been placed on the renin-angiotensin system. It seems clear that the response to renal artery stenosis differs among species. In man, there is considerable evidence for a primary role for the renin-angiotensin system in chronic renal hypertension, whereas in the dog, rabbit, and rat the pathogenic mechanisms appear to differ. Also, there is an increasing body of evidence which suggests that humoral mechanisms other than the renin-angiotensin system are important in the pathogenesis of hypertension secondary to renal artery constriction in the dog. rabbit, and rat. These animal models of renal hypertension serve a very useful role in the investigation of the mechanisms operative in the patient with renovascular hypertension. It is the purpose of this review to present an analysis of the data bearing on the possible primary pathogenic mechanisms in renovascular hypertension.