P otassium has been shown to suppress plasma renin activity (PRA). This study was designed to study the role of increased aldosterone production in the mediation of such a response. Five patients with adrenal insufficiency were placed on a diet of 60 meq potassium and 100-150 meq of sodium while receiving a constant amount of cortisone acetate and Florinef. Upright PRA was determined each day for 2-3 days in the control period and then for 3-4 days after potassium intake had been increased to 200-300 meq/day. Potassium loading induced a natriuresis. Hence, patients were either sodium replaced (six studies in four patients) or allowed to become sodium depleted (three patients). Potassium loading without replacement was associated with a decrease in weight, negative sodium balance, hyperkalemia, and a positive potassium balance. PRA rose during the experimental period. Potassium loading with sodium replacement was associated with little change in weight or sodium balance. Hyperkalemia and positive potassium balance were present to the same degree as found in the studies without sodium replacement. When all PRA values are considered (both morning and evening values) there was no significant change with potassium loading (+ 1.31 ng/ml per h; range + 6.9 to -2.0). We conclude that hyperkalemia or a positive potassium balance did not suppress PRA in Addisonian man in these studies when sodium balance was maintained, nor did it prevent a rise in PRA when sodium balance was negative.