Mechanisms of Catecholamine Inactivation by the Endocrine Pancreas

The present study was designed to determine if mechanisms are present in the islets of Langerhans to inactivate catecholamines. The dopamine content of the pancreatic beta cells was increased by incubating rabbit pancreas segments with L-3, 4-dihydroxyphenylalanine (L-dopa) for forty-five minutes prior to stimulation with glucose, 16.5 mM. Monoamine oxidase (MAO) inhibitors (pargyline, tranylcypromine and harmine) potentiate the inhibition of insulin secretion by increased beta cell dopamine, but not by dopamine added to the incubation media. Catechol-Omethyltransferase (COMT) inhibitors (pyrogallol and tropolone) did not potentiate the inhibition of insulin secretion from rabbit pancreas by beta cell dopamine. Isolated islets obtained from rabbits, rats, and golden hamsters contained MAO; only golden hamster, a species with a rich intrainsular adrenergic plexus, had COMT in their islets. Compounds that inhibit cellular uptake of catecholamines (cocaine, nortryptyline, and imipramine) potentiate the inhibition of insulin secretion resulting from the presence of norepinephrine in the incubation media but not the inhibition resulting from increased beta cell dopamine. The present study suggests that MAO and beta cell catecholamine uptake may play a role in the inactivation of catecholamines by the islets of Langerhans.