EFFECT OF PHARMACOLOGICAL AGENTS AND FASTING ON PANCREATIC-ISLET NOREPINEPHRINE IN THE GOLDEN-HAMSTER

Using a specific and sensitive radioenzymatic assay that utilizes the partially purified enzyme phenylethanolamine-N-methyltransferase, studies were done to determine if pharmacological agents and/or fasting alter the norepinephrine [NE] concentration of collagenase-isolated golden hamster pancreatic islets. The NE concentration (42.1 .+-. 8.07 .mu.mol/kg net wt, mean .+-. SE) and the monoamine oxidase [MAO] activity (5407 .+-. 530 pmol product/mg tissue per min) of hamster pancreatic islets was at least 5 times higher than acinar pancreas, kidney, heart, median eminence or cerebral cortex. The catechol-o-methyltransferase activity of hamster islets (7 .+-. 2.3 pmol product/mg tissue per min) was one half or less than the other tissues. Islet NE was not increased by 2 days administration of the MAO inhibitor tranylcypromine. Islet NE concentration was increased 2-fold by administration of the NE precursor DL-threo-dihydroxyphenylserine. This increase was enhanced by prior administration of tranylcypromine (3.5-fold) and prevented by prior administration of the decarboxylase inhibitor N1-(DL-seryl)-N2-(2,3,4-trihydroxybenzyl) hydrazine (RO-4-4602). There was a good correlation between the islet NE concentration and the plasma glucose concentration after pharmacological agents. Reserpine administration markedly depleted the islet NE concentration. Fasting of 24, 48 and 72 h did not alter the NE concentration in islets and heart. The pancreatic islets of the hamster have an active noradrenergic system, but islet NE does not appear to play an important role in the impaired insulin secretion of fasting hamsters.