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Abstract
The hypertension, which had previously been observed 3 months after the experimental
production of unilateral renal arterial stenosis, has been shown to persist throughout
a 6 month period of observation. In 2 hypertensive animals the kidneys were small
and scarred, and renal blood flow was reduced. In the other 3 hypertensive dogs, the
renal mass was moderately reduced, and renal blood flow per unit of kidney weight
was normal. The distal renal artery pressures and pulse pressures were within the
normal range.
When the contralateral kidney was excised 5 to 7 days after production of renal artery
stenosis, most of the animals died. The 12 surviving animals were hypertensive, and
in 10 of them the test kidney was markedly hypertrophic 3 months later. In these animals,
too, the distal renal artery pressure and pulse pressures were within the normal range.
Renal blood flow was normal or slightly increased when calculated in cubic centimeters
per gram of renal tissue.
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References
- Studies on the etiology of renal hypertension.Ann. Surg. 1937; 106: 826
- Experimental unilateral renal artery stenosis.Surg. Gynec. & Obst. 1962; 114: 415
- Studies on experimental hypertension. The production of persistent elevation of systolic blood pressure by means of renal ischemia.J. Exper. Med. 1934; 59: 347
- Influence of renal denervation upon renal blood flow.Surg. Gynec. & Obst. 1960; 110: 622
- Persistent hypertension in the dog following disruption of the carotid sinus nerves and subsequent unilateral renal artery constriction.Circulation Res. 1960; 8: 934
- Experimental hypertension: Observations on sustained elevation of systolic and diastolic blood pressure in dogs.J. Clin. Invest. 1936; 15: 543
Article info
Publication history
Received:
February 9,
1962
Footnotes
☆Aided by grants from the American Heart Association, the James Whitcomb Riley Memorial Association, and by Public Health Service Research Grant H-203 C5 from the National Heart Institute, National Institutes of Health, Public Health Service.
Identification
Copyright
© 1962 Published by Elsevier Inc.
