It has been generally recognized that the secretion of aldosterone is mainly regulated by angiotensin II in animals and humans, however, potassium and ACTH are also proposed as other humoral factors involved in the aldosterone secretory process. Recently, stress, anesthesia, adrenergic stimulation, low sodium intake or water deprivation stimulate plasma renin activity, while high sodium intake and deoxycorticosteroid have been reported to cause suppression of renin activity in animals. It seems that overall response of aldosterone secretory mechanisms reflects complex interactions both intrarenal and extrarenal components. Furosemide has been widely used to investigate the control of renin secretion by the kidney, and the relationship between diuretics and the disposition of endogenous aldosterone were reported (Oh, 1984). The sequential with 10 min interval samples of plasma were collected following administration of furosemide(1 mg/kg), aspirin(10 mg/kg), respectively. And also similar experiment was performed in the propranolol (10 mg/kg) pretreated rabbits. The results were as follows : 1) The concentration of plasma aldosterone was average of 426.I ~ 485.5pg/ml in normal rabbits. Plasma concentrations of aldosterone rised significantly after injection of furosemide during 50 min, and the rise of plasma aldosterone was blocked by the propranolol pretreatment 2) Significant fall in the plasma level of aldosterone after injection of aspirin was noted. This result indicates that the increased secretion of aldosterone induced by furosemide administration is mediated through β-receptors, and the possible role of prostaglandin is substantiated.