DIFFERENT MECHANISMS ARE INVOLVED IN NEUROPEPTIDE Y-INDUCED PANCREATIC VASOCONSTRICTION AND INHIBITION OF INSULIN-SECRETION

We have studied the mechanisms whereby neuropeptide Y (NPY) inhibits i nsulin secretion and induces vasoconstriction in the isolated perfused rat pancreas. Neither prazosin (alpha1-adrenoceptor antagonist; 6 muM ) nor yohimbine (alpha2-adrenoceptor antagonist; 0.6 muM) affected the effects of neuropeptide Y (1 nM). Also the Ca2+ channel antagonist, v erapamil (5 muM), which itself decreased insulin output by 55%, could not affect the neuropeptide Y-induced inhibition of insulin secretion. However, verapamil impaired the neuropeptide Y-induced decrease in pa ncreatic outflow rate. Finally, neuropeptide Y (1 and 10 nM) suppresse d the insulin secretion induced by dibutyryl cAMP (100 muM) and the cy clic nucleotide suppressed the neuropeptide Y-induced vasoconstriction . We conclude that the secretory and vascular effects of neuropeptide Y are mediated by different processes in the perfused rat pancreas: in hibition of insulin secretion seems mediated by a mechanism distal to and/or different from cAMP generation, whereas vasoconstriction seems to involve uptake of extracellular Ca2+ and to be sensitive to dibutyr yl cAMP. Both effects occur independently of adrenoceptor receptors.