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Abstract
Chronic experimental renal hypertension in dogs has been successfully treated with
crude and semipurified hog renins and chronic experimental renal hypertension in dogs
has been prevented by prophylaxis with crude and semipurified hog renins.
These therapeutic and prophylactic effects are well-correlated with the antirenin
titer. This evidence for antirenin (or an antibody to a protein closely related to
renin) as the mechanism of the antihypertensive effects of hog renins constitutes
support for the affirmative of the long-standing controversy regarding the primary
role of renin (or some closely related protein) in the pathogenesis of experimental
renal hypertension.
Hog renal medulla contains a factor which interferes with the antihypertensive effects
of hog renin in experimental renal hypertension in the dog by a mechanism presently
unknown.
Renotoxic and renal protective factors have been found to occur in fractions of renal
extracts. Toxicity consists in increased and protection in decreased incidence of
uremia after constriction of the renal arteries.
After further preliminary experiments in animals, the possible pathogenetic role of
the kidney in essential hypertension will be studied by passive immunization of patients
with purified antirenin to human renin.
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References
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Article info
Publication history
Received:
July 7,
1952
With the Technical Assistance of E. Henrioulle, B.S., M. Chaparro and Bradley Keith∗∗∗∗During the past twelve years, other members of the research team responsible for this work were: H. E. Bessinger, T. L. Brannick, R. O. Burns, R. G. Canham, G. R. Chobot, W. Donaldson, D. Frankel, W. Gaines, M. L. Goldberg, B. Gomberg, E. W. Hawthorne, R. M. House, C. A. Johnson, J. P. Kiely, J. M. Kiely, O. Kamm, E. H. Lambert, J. Marshall, C. J. Marienfeld, J. J. Milford, J. B. Moore, W. G. Moss, G. Olander, B. G. Osgood, E. A. Ohler, E. L. Propes, M. R. Salk, J. J. Schwab, R. W. Sevy, E. L. Smith, R. Walker, J. R. Weir, and M. Yanowitz, and the following technicians: F. Kajikawa, T. Lefco, H. Minatoya, T. Patton, J. M. Silva, M. C. Tanner, and R. E. Vessey.Footnotes
☆This investigation is presently supported by the National Heart Institute of the United States Public Health Service (Grant H-428 C-3), the American Heart Association, the Chicago Heart Association, and the University of Illinois Foundation. During the past ten years, this research has been supported by the National Heart Institute, the Markle Foundation, the United States Navy, the American Foundation for High Blood Pressure, and the Graduate College Research Board of the University of Illinois.
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Copyright
© 1953 Published by Elsevier Inc.
