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Renal artery constriction induces hypertension experimentally; leaves open its relevance to human disease; clinical studies required.
Interest in the relation of renal function and arterial hypertension, recognized since the time of Bright, has been greatly stimulated by the experimental work of Goldblatt and his associates,1who were able to produce permanent hypertension in animals by partial constriction of the main renal arteries. The experiments of Goldblatt and his co-workers have been successfully repeated in different ways by many authors, as cited by Goldblatt,2and the importance of normal renal circulation for the maintenance of normal blood pressure in animals appears to be an established fact. Page and his associates3and Muñoz and Braun-Menendez and their associates,4reviving the original work of Tigerstedt and Bergman,5have offered further evidence of the importance of the renal circulation in hypertension by demonstrating the production in the kidney of a pressor substance, which they have called angiotonin, or hypertensin. The amount of angiotonin produced is increased when
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Piero P. Foà (1942) studied this question.
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