We have succeeded in producing sustained benign hypertension in stumptail macaques (Macaca arctoides) by unilateral renal artery narrowing. The critical degree of constriction was achieved by monitoring renal blood flow with an electromagnetic flowmeter and reducing flow to 75 percent to 85 percent of normal. The uninvolved kidney was left in situ, thus creating a two kidney primate model of renal hypertension. Monkeys had been kept on an atherogenic cholesterol, coconut-peanut-oil diet for three months before operation and, after the renal artery clipping, were continued on diet for six additional months. Some were to be killed at this time to serve as baseline controls. Two groups of six monkeys had their diet changed to low-fat monkey chow. One of the two groups was made normotensive by nephrectomy of the ischemic kidney. Evolution of lesions will be compared to those of the baseline control group and to each other. In addition we plan to study the effect of treatment of hypertension (i.e., nephrectomy) on the evolution of aortic and coronary atherosclerosis while continuing the atherogenic diet. We will then compare all five groups that will constitute this study. These groups were begun during the past year and the results are still incomplete. Another study dealt with the influence of three different drugs on diet-induced atherosclerosis in stumptail macaques. The drugs used were clofibrate, a hypolipidemic drug, propranolol, a beta-adrenergic blocking agent, and minoxidil, an antihypertensive drug of the vasodilator group. The results suggest that clofibrate and propranolol have a beneficial action on diet-induced atherosclerosis, whereas minoxidil has no enhancing or ameliorating effect on the response to the atherogenic diet.