Studies on the Role of Adenylcyclase in Insulin Secretion

Abstract
The administration of glucose, tolbutamide, corticotropin, and glucagon to mice resulted in stimulation of insulin secretion. These stimulations were all inhibited by the prior administration of β-adrenergic receptor blocking agents. Cyclic 3',5' adenosine monophosphate stimulated insulin secretion in intact mice and its stimulatory effect was also inhibited by β-adrenergic receptor blocking agents. The locus of the inhibitory effects of β-adrenergic receptor blocking agents on insulin secretion is discussed.