Abstract

It has now been >100 years since the seminal observations of Professor Tigerstedt and his medical student–colleague, Bergmann, demonstrated the pressor effects of renal extracts.1 The clinical relevance of these observations became more apparent with the classical experiments of Harry Goldblatt and his colleagues who demonstrated in the 1930s that inducing renal ischemia by ligation of a renal artery could cause hypertension in dogs.2 The identification of renin and angiotensin in the laboratories of Page and Helmer in Indianapolis3 and, virtually simultaneously, by Braun-Menendez and Fasciolo in Buenos Aires, Argentina,4 elucidated the mechanism involved. The search for human counterparts of the experimental paradigm by which renal ischemia led to hypertension and its potential remediation soon followed with the application of the tedious biological assay for renin to venous blood samples obtained from the kidneys with stenotic lesions in vivo by Judson and Helmer.5 This introduced an era, encompassing the past 40 years, when the possibility of correcting this increasingly recognized secondary form of hypertension became feasible. A variety of techniques have now been devised to detect abnormalities of renal blood flow and to attempt to correct them by surgical means or with a variety of vascular interventions when found. Although ischemic lesions of the main renal artery have received the overwhelming majority …

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