Abstract
Ischemia of the dog's kidney, produced by constriction of the renal arteries, results in a chronic hypertension (Goldblatt, Lynch, Hanzal and Summerville 1 ). Destruction of the nerves to the kidney does not prevent the development of this hypertension (Page, 2 Collins 3 ). Hence it may be supposed that we are dealing with a chemical mechanism. A number of workers (Prinzmetal and Friedman 4 ; Harrison, Blalock and Mason 5 ; Govaerts and Dicker 6 ) have reported that extracts from the kidneys of dogs with such experimental renal hypertension exert a greater pressor effect than similar extracts from normal kidneys. This finding leads one to believe that the hypertension is due to the liberation of pressor substances into the blood stream from the ischemic kidney. The theory would be greatly supported if increased amounts of pressor substance could be demonstrated in the blood. Dicker 7 in fact reports that the blood of such dogs contains a hypertensive substance, while that of normal dogs does not. However, Page 8 could not find increased pressor substances. Alcohol extracts of the plasma of such dogs, when injected into cats, showed no more pressor activity than similar extracts made from normal plasma. We have attempted in this investigation to demonstrate increased pressor substances in the blood by massive transfusions from large dogs with renal hypertension into small normal dogs. The results have been entirely negative.
The hypertension in the donor dogs was produced by constriction of the renal arteries by a method described previously (Collins 3 ). The systolic blood pressures of these animals varied from 180 to 230 mm. Hg. These dogs were large (20–30 kg.), and small dogs (4.5–9 kg.) were chosen as recipients in order that large amounts of blood, in relation to the size of the animal, could be injected.
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