Abstract
In preliminary experiments by Goldblatt, 1 bilateral adrenalectomy in dogs appeared to interfere with the development or maintenance of the hypertension which follows experimental production of renal ischemia. Similar results were obtained by Blalock and Levy 2 and by Page. 3 On the other hand, Collins and Wood 4 concluded that, “It is unlikely that the adrenal cortex is involved specifically in the etiology of experimental renal hypertension other than in the sense that the cortex is important in the maintenance of blood pressure in normal as well as in hypertensive states.”
Our experiments show that this form of experimental hypertension can exist in the complete absence of the adrenal glands, in untreated animals. Seven dogs were subjected to complete bilateral adrenalectomy in addition to constriction of the main renal arteries by means of Goldblatt clamps. Four of these animals were treated by administration of salt (sodium chloride and citrate, occasionally also bicarbonate) alone or in addition to a commercial extract of adrenal cortex.† In 3 experiments no treatment whatever was employed and the use of salt for seasoning food was avoided. All the blood pressure observations were made by the carotid loop (Van Leersum) method. The cuff was adjusted by the same observer in every case and not less than 12 readings were recorded each time.
Following excision of the second adrenal, in hypertensive dogs, a decided fall of blood pressure sometimes occurs within a day. We have observed a similar fall of pressure in some hypertensive animals after operations other than adrenalectomy. Our experience has shown that return to hypertensive levels of pressure can occur in such adrenalectomized dogs without administration of salt or adrenal extract. The rise in pressure, therefore, cannot be attributed, with confidence, to treatment when given.
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