NEURAL REGULATION OF PEPTIDE-YY SECRETION

The purpose of these experiments was to investigate the neural control of peptide YY (PYY) secretion. The effects of various pharmacological manipulations and vagotomy on peptide YY (PYY) secretion was examined in dogs. Atropine, hexamethonium and atropine plus hexamethonium treatment blocked food-induced release of PYY significantly. Integrated release of PYY in response to food alone and in combination with atropine, hexamethonium and atropine plus hexamethonium were 8.8 +/- 2.2, -1.1 +/- 2.3, -2.7 +/- 2.2 and -3.2 +/- 3.1 (ng (0-150) min/ml), respectively. Beta-adrenergic blockade with propranolol or depletion of nerve terminal stores of catecholamines with reserpine did not affect food-stimulated release of PYY. Truncal vagotomy resulted in significant elevations of basal and food-induced release of PYY. IV administration of bethanechol, a cholinergic agonist, and electrical stimulation of the vagus nerve resulted in release of PYY. Together, these data suggest that food-stimulated PYY secretion is dependent on ganglionic transmission and an atropine-blockable postganglionic parasympathetic pathway; and that PYY release is inhibited tonically, probably through a vagal cholinergic mechanism. Adrenergic pathways do not participate in food-stimulated PYY release; however, electrical stimulation of the splanchnic nerves increased basal levels of PYY, suggesting that the sympathetic nervous system affects release of PYY.