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S.V.

JAMA. 1970;213(11):1889-1890.

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When in 1934 Goldblatt began his classic experiments on canine kidneys his intention was to confirm a hypothesis on renal origin of essential hypertension. The results failed to support this theory, but, unexpectedly, the experimental hypertension induced by renal artery constriction disclosed the ischemic mechanism responsible for hypertension in renal vascular disease. Almost inadvertently Goldblatt had "rediscovered" renin, establishing it as the hormonal mediator in renal hypertension.

Recent evidence would suggest that the concept of renal hypertension may have to be expanded to include essential hypertension in its malignant phase. Onesti and his co-workers¹ studied six uremic patients with malignant hypertension before and after bilateral nephrectomy. All patients had had benign essential hypertension for several years before the onset of the accelerated phase, and in none was there any evidence of primary renal vascular or parenchymal disease. In all six patients the clinical course of the systemic blood pressure . . . [Full Text PDF of this Article]

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