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PIERO P. FOÀ, M.D., Ph.D.; WARD W. WOODS, M.D.; MAX M. PEET, M.D.; NAOMI L. FOÀ, B.A.

Arch Intern Med. 1942;69(5):822-835.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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,¹ who 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,² and the importance of normal renal circulation for the maintenance of normal blood pressure in animals appears to be an established fact. Page and his associates³ and Muñoz and Braun-Menendez and their associates,⁴ reviving the original work of Tigerstedt and Bergman,⁵ have 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 . . . [Full Text PDF of this Article]

Author Affiliations
ANN ARBOR, MICH.

Footnotes
Mendelson Research Fellow.

Funds for this work were made available through a grant to the Department of Neurosurgery by the Aaron Mendelson Memorial Trust Fund.

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