Interactions of islet hormones with acetylcholine and cholecystokinin-octapeptide in the isolated pancreas of normal and diabetic rats

Abstract

This study investigates the effects of the neuropeptides, vasoactive intestinal polypeptide (VIP) and galanin, the islet hormones insulin, glucagon and somatostatin, the neurotransmitter acetyicholine (ACh), the gut hormone cholecystokinin octapeptide (CCK-8), sodium nitroprusside (SNIP), 8-Bromo guanosine 3'5' cyclic monophosphate (8-Br cOMP) and nerve stimulation on amylase secretion and intracellular free calcium concentration ([Ca 2 ]) in the isolated pancreas of normal and diabetic rats. The pattern of distribution of the islet hormones and neuropeptides in normal and diabetic rats. The results show that stimulation of isolated pancreatic segments and acinar cells with different concentrations of either glucagon, somatostatin, VIP, galanin, ACh or CCK-8 resulted in different effects on amylase secretion and [Ca 2']i Combining the islet
hormones with either ACh or CCK-8 resulted in marked potentiation in amylase output and enhanced the [C2] in acinar cells. Genistein, had markedly inhibited the potentiation of the islet hormones with either ACh or CCK-8. Similarly, when rats were rendered diabetic either insulin, glucagon or somatostatin failed to potentiate the secretory response of ACh or CCK-8. The results indicate that both tyrosine kinase and cellular C2 seem to be the intracellular mediators involved with the enhanced
secretory responses obtained with a combination of the islet hormones with either ACh or CCK-8. Immunohistochemiocal techniques confirm the presence of the islet hormones and neuropeptides in the endocrine and the neural elements of the pancreas.
Moreover, the presence of viable pancreatic islets of Langerhans seems to be associated with the potentiation of the islet hormones with either ACh or CCK-8. The results also suggest that NO may modulate the release of the endogenous neurotransmitter(s) in response to EFS in the exocrine rat pancreas.