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Central and peripheral neural control of pancreatic exocrine secretion

100%

Niebergall-Roth E. , Singer M. V.

tom 52

nr 2

Neural control of the release and action of secretin

84%

Chey W. Y. , Chang T-M.

nr 4

105-112

The release and physiological actions of secretin on pancreatic exocrine secretion and gastric secretion of acid and motility are regulated by neuro-hormonal control. The release of secretin by duodenal acidification is mediated by a secretin releasing peptide (SRP). The release and action of SRP are neurally mediated depending on vagal afferent pathway. SRP activity in acid perfusate of the duodenum was substantially decreased when rats were treated with tetradotoxin (TTX), perivagal application of capsaicin, a ß-adrenergic blocker, Met-enkephalin (MEK) or vagotomy. The release of secretin by SRP was abolished in rats treated with TTX, mucosal or perivagal application of capsaicin, MEK or vagotomy. Both release of secretin and pancreatic exocrine secretion (PES) elicited by duodenal acidification were also inhibited dose-dependently by Met-enkepahlin, 5-HT2 antagonist, ketanserin and 5-HT3 antagonist, ondansetron. Stimulation of PES and inhibition of gastric acid secretion and motility by secretin in a physiological dose are also dependent on the vagal afferent pathway as these effects of secretin are abolished by perivagal capsaicin treatment or vagotomy. In conscious rats, vagotomy, vagal ligation, or perivagal colchicine but not capsaicin treatment reduced the number of secretin binding sites in the forestomach suggesting another mode of neural regulation that affects gastric motility. Except in the rat, stimulation of PES by secretin in a physiological dose is profoundly inhibited by atropine indicating the importance of a cholinergic input. In isolated and perfused rat pancreas, electrical field stimulation potentiated secretin-stimulated PES that was suppressed by atropine and anti-GRP serum, suggesting the roles of intrapancreatic cholinergic and GRP-containing neurons. In rats, secretin-stimulated PES was inhibited by a NO synthase inhibitor suggesting mediation by NO. However, the neuropeptides and neurotransmitters involved in regulation of the release and action of secretin and their sites of action remain to be elucidated.

Central and peripheral neural control of pancreatic exocrine secretion

84%

Niebergall-Roth E. , Singer M. V.

nr 4,1

Efferent vagal impulses act on the exocrine pancreas via pancreatic ganglia, where the impulses are modulated and modified, and terminate via postganglionic fibers at the acinar cells. Acinar muscarinic receptors of the subtype M1 play an important role for the mediation of the stimulatory vagal influences on pancreatic exocrine secretion. In dogs, a potentiative interaction exists between the two most important mediators of the pancreatic exocrine response to intraduodenal stimuli, efferent vagal impulses and CCK. In contrast to humans and rats, in which all action of CCK on pancreatic enzyme output is vagally mediated, CCK acts in dogs in part as a classical humoral factor independent of the cholinergic system. Although several peptides found in pancreatic nerve cell bodies or fibers can stimulate or inhibit pancreatic exocrine secretion, their physiological importance in the neural control of the exocrine pancreas needs to be further evaluated.