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Litten ( 1 ) observed in 1881 that temporary occlusion of the renal artery in dog and rabbit for 11/2 to 2 hours was followed by tubular necrosis. In 1926 McEnery, Meyer and Ivy (2) clamped the blood vessels of both kidneys in dogs for periods of 30 minutes to 1 hour. This led to an increase in BUN 2 and some animals died in uremia. Recently, Emmel (3) described the mitochondrial and pH changes in the rat's kidney following interruption and restoration of the renal circulation. Scarff and Keele (4) removed the right kidney of rabbits and then clamped the left renal pedicle for periods up to 120 minutes. After release the BUN rose rapidly until death or reached a peak and declined with recovery. Outcome did not always depend on time of occlusion. Van Slyke et al (5) found that in the dog, if one kidney was removed and the renal artery of the other clamped for 3 hours, the animal would recover following an elevation of BUN. With clamping of 4 hours, only half of the dogs recovered and at 6 hours the procedure was Uniformly fatal with uremic death in 4 to 8 days. Thus renal occlusion of more than 4 hours was considered irreversible. Selkurt (6) studied the effect of temporary clamping of the left renal artery of the dog on subsequent left renal clearances. Ischemia of 20 minutes' duration practically eliminated creatinine and paraamino-hippuric acid clearances during observations extending for 136 minutes after release of clamp.In the following experiments a study was made of the effects of temporary complete renal ischemia in rats. With aseptic technique the kidneys were then exposed by lumbar incisions extending through the oblique abdominal muscles, the renal pedicles isolated, and the renal artery and vein occluded by means of bulldog clamps. The latter were applied on right and left sides usually within an interval of 20 seconds. Ureters were not occluded. Except for separation of adrenal from the kidney, no dissection of peri-renal fat was made. In all rats 0.5 ml. heparin was injected into the tail vein about 10 minutes before clamping to retard intrarenal thrombosis during the period of vascular occlusion. The heparin did not cause excessive bleeding. Food and water were withheld for about 10 hours prior to anesthesia, and were given ad libitum following the operation.Complete renal ischemia was maintained bilaterally for exact periods of time, i.e., 30 minutes, 1 hour, 90 minutes, and 2 hours. The kidneys were generally dark purple at the end of these periods, but all became uniformly pink either within a matter of seconds or a few minutes after removal of the clamps. A group of 15 rats was studied at each time interval.Renal function was followed by determination of BUN, made according to the method of Ormsby (7) with 0.1 or 0.2 ml. of blood from the tail. A control level was obtained prior to operation and then values were determined at fixed intervals following removal of the clamps, i.e., 6 hours, 24 hours, 2, 3, and 4 days, and in some instances 6 and 8 days. A sample of heart's blood was taken for ...

1. Infusion of sufficient renin to raise the blood pressure of normal rats to hypertensive levels resulted in increased renin in the arterial wall. 2. Arterial wall renin and renal venous renin were normal in younger spontaneously hypertensive rats, but in older spontaneously hypertensive rats arterial wall renin was significantly increased and renal venous renin was significantly decreased. 3. Arterial wall renin in rats with either acute or chronic two-kidney Goldblatt renal hypertension was significantly increased, whereas circulatory renin was elevated in the former, but depressed in the latter. 4. Arterial wall renin may play a role in the maintenance of acute and chronic renal hypertension and also perhaps of spontaneous hypertension of long duration in older rats.