Electrical stimulation of vagus nerves (ESV) increases pancreatic exocrine secretion. In the present study, we have investigated in the rats that possible roles of peptides such as cholecystokinin (CCK), secretin, vasoactive intestinal polypeptide (VIP), pituitary adenylate cyclase activating peptide (PACAP), insulin, gastrin releasing peptide (GRP) and somatostatin on ESV-induced pancreatic secretion. Under the Ձ-chloralose anesthesia, pancreatic juice was collected to determine volume and protein, while distal ends of truncal vagi were stimulated for 15 min using a current of 9 V, 10 cps and 5 ms. After 30 min, stimulation was repeated under the systemic administration of several peptide antagonists or polyclonal antibodies (Ab). Blood was collected from aorta to measure plasma levels of CCK-8, VIP, PACAP, insulin, GRP, somatostatin, gastrin, and secretin. ESV produced a significant increase in the pancreatic secretion. The increase in pancreatic secretion paralleled the increases in plasma CCK-8, VIP, PACAP, insulin, GRP, somatostatin, gastrin but not secretin. ESV-induced pancreatic flow volume and protein output were significantly inhibited, but partially, by CCK-A receptor antagonists (loxiglumide, L364,718), anti-VIP Ab, PACAP antagonist (PACAP6-38), anti-PACAP Ab, anti-insulin Ab and anti-GRP Ab but not by CCK-B receptor antagonist (L365,260) and anti-somatostatin Ab. Hexamethonium completely abolished ESV-induced pancreatic secretion whereas atropine produced 72% inhibition of ESV-induced pancreatic flow volume. The present study indicates that pancreatic exocrine secretion induced by ESV in rats is mediated by several neuropeptides including CCK, VIP, PACAP, GRP and insulin which require intact nicotinic receptor to exert their actions. Furthermore, ESV-induced pancreatic secretion is mediated by both cholinergic and peptidergic nerve pathway.

Keywords: vagally-mediated pancreatic secretion, neuropeptides, cholinergic, peptidergic