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November 30, 1940


JAMA. 1940;115(22):1889-1890. doi:10.1001/jama.1940.02810480053014

From a study of the hemodynamics of the perfused isolated canine kidney, Kohlstaedt and Page1 of the Lilly Laboratory for Clinical Research, Indianapolis, have formulated a definite theory as to the method of production of arterial hypertension, subsequent to experimental renal ischemia.

Six years ago Goldblatt and his co-workers2 of the Institute of Pathology, Western Reserve University, proved that in dogs renal ischemia caused by bilateral compression of the renal arteries is almost invariably followed by a definite and persistent elevation in systolic blood pressure. Since this secondary hypertension is not prevented by preliminary denervation to the kidneys, it seemed logical to assume that it is due to some unknown retention product or internal secretion from the kidneys. Transplantation of ischemic kidneys into normal dogs confirmed the so-called internal secretion theory. Much experimental and clinical evidence seems to indicate that renin may be the pathologic internal secretion responsible