The beta-adrenergic blocking agent propranolol had in itself no notable influence on the blood glucose level in rats, but in combination with chlorpropamide it considerably delayed and enhanced the hypoglycaemic and liver glycogenolysis depressing actions of chlorpropamide. This effect was still more pronounced when the rats were treated in addition to propranolol and chlorpropamide with thyroxine or glanduitrine, which in themselves act as stimulators of liver glycogenolysis. The simultaneous administration of propranolol and chlorpropamide depressed considerably the liver glycogenolysis induced by prolonged fasting and inhibited completely the liver glycogenolysis observed after hepatectomy. The reports available in the literature on propranolol-precipitated hypoglycaemia in patients are surveyed and it is supposed that the beta-adrenergic blocking agent produces hypoglycaemia primarily through the depression of liver glycogenolysis. This observation supports the hypothesis that the adrenergic beta-receptors play an important role in the sympathetic control of liver glycogenolysis.