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LIEUTENANT JEROME A. GANS

Arch Ophthal. 1944;32(4):267-275.

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

Considerable impetus was given to the study of hypertension when Goldblatt¹ showed that persistent hypertension could be produced experimentally in dogs by partial clamping of the renal artery. The years that followed brought an extensive literature, based on a renal origin of hypertension. Page² showed that persistent hypertension could also be induced by enclosing the kidney in a sac of cellophane, which produced a constricting capsule of scar tissue. The "ischemic" kidney was shown to contain increased amounts of a substance, renin,³ which combined in the circulation with a renin activator to produce angiotonin, a pressor substance.⁴ Then it was found that normal kidney tissue contained an antipressor substance that inactivated angiotonin; this was used by Page and associates⁵ to treat hypertensive patients and experimental animals. Thus, various humoral factors and antifactors have come to light.

A different point of view was presented when Heymans . . . [Full Text PDF of this Article]

Author Affiliations
MEDICAL CORPS, ARMY OF THE UNITED STATES

From the Division of Ophthalmology, Department of Surgery of the University of Chicago.

Footnotes
Read at a meeting of the Chicago Ophthalmological Society, March 15, 1943.

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