In the earliest studies on experimental hypertension due to renal ischemia1 it was shown that constriction of the main artery of only one kidney in a dog or a monkey is sufficient to cause elevation of the blood pressure. It was also shown in these and in later studies2 that this elevation does not usually persist indefinitely unless the other kidney is removed or unless the main artery of the other kidney is also constricted. In most dogs with unilateral renal ischemia the blood pressure returns to the preoperative level in six weeks or less, but in some the hypertension may persist at a high level for many months. The return of the blood pressure to normal obviously may be due (a) to the development of considerable accessory circulation to the ischemic kidney or (b) to the compensating, neutralizing or inhibiting effect of the contralateral normal kidney. The