Control of pancreatic exocrine secretion via muscarinic receptors: Which subtype(s) are involved?

Niebergall-Roth, Elke; Singer, Manfred V.

doi:10.1159/000071766

Cited by 13 publications

(12 citation statements)

References 46 publications

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“…In fact, the acinar cell was thought to lack an M1 muscarinic receptor. More recently, the results published in the literature [35] clearly demonstrate the existence of both subtypes on acinar cells. What is more, Schmid et al [36] have shown that carbachol-induced amylase secretion in isolated acinar cells was more potently inhibited by the M1-selective antagonist telenzepine than by M3-selective antagonists.…”

Section: Discussionmentioning

confidence: 79%

Effects of the type of dietary fat on acetylcholine-evoked amylase secretion and calcium mobilization in isolated rat pancreatic acinar cells

Yago

Diaz

Martínez

et al. 2006

The Journal of Nutritional Biochemistry

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Section: Discussionmentioning

confidence: 79%

Effects of the type of dietary fat on acetylcholine-evoked amylase secretion and calcium mobilization in isolated rat pancreatic acinar cells

Yago

Diaz

Martínez

et al. 2006

The Journal of Nutritional Biochemistry

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“…A series of in vivo studies in human and dogs also indicated that telenzepine can inhibit basal and stimulated pancreatic exocrine output with high potency (for a recent review of these studies, see Niebergall-Roth and Singer, 2003). Based on these findings it has been proposed that M 1 receptors play an important role in regulating pancreatic exocrine secretion (Niebergall-Roth and Singer, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…Based on these findings it has been proposed that M 1 receptors play an important role in regulating pancreatic exocrine secretion (Niebergall-Roth and Singer, 2003). However, radioligand binding studies indicate that telenzepine not only binds to M 1 receptors with high affinity (K i ϳ1 nM) but also shows relatively high affinity for M 3 receptors (K i ϳ 4 -8 nM; Schudt et al, 1989;Lazareno et al, 1990;Karton et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

Cholinergic Stimulation of Amylase Secretion from Pancreatic Acinar Cells Studied with Muscarinic Acetylcholine Receptor Mutant Mice

Gautam¹,

Han²,

Heard³

et al. 2005

J Pharmacol Exp Ther

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Muscarinic acetylcholine receptors (mAChRs) expressed by pancreatic acinar cells play an important role in mediating acetylcholine-dependent stimulation of digestive enzyme secretion. To examine the potential roles of M 1 and M 3 mAChRs in this activity, we used M 1 and M 3 receptor single knockout (KO) and M 1 /M 3 receptor double KO mice as novel experimental tools. Specifically, we examined the ability of the muscarinic agonist carbachol to stimulate amylase secretion in vitro, using dispersed pancreatic acini prepared from wild-type and mAChR mutant mice. Quantitative reverse transcription-polymerase chain reaction studies using RNA prepared from mouse pancreatic acini showed that deletion of the M 1 or M 3 mAChR genes did not lead to significantly altered mRNA levels of the remaining mAChR subtypes. Moreover, immunoprecipitation studies with M 1 and M 3 mAChR-selective antisera demonstrated that both mAChR subtypes are expressed by mouse pancreatic acini. Strikingly, carbachol-induced stimulation of amylase secretion was significantly impaired in acinar preparations from both M 1 and M 3 receptor single KO mice and abolished in acinar preparations from M 1 /M 3 receptor double KO mice. However, another pancreatic secretagogue, bombesin, retained its ability to fully stimulate amylase secretion in acinar preparations from M 1 /M 3 receptor double KO mice. Together, these studies support the concept that cholinergic stimulation of pancreatic amylase secretion is mediated by a mixture of M 1 and M 3 mAChRs and that other mAChR subtypes do not make a significant contribution to this activity. These findings clarify the long-standing question regarding the molecular nature of the mAChR subtypes mediating the secretion of digestive enzymes from the exocrine pancreas.

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“…88 Furthermore, enzyme secretion in the autotransplanted pancreas in response to intestinal stimulants is unaltered by vagotomy or atropine, whereas the intact pancreas is strongly inhibited by each of these maneuvers. 94 In summary, there is good evidence for direct cholinergic stimulation of pancreatic enzyme secretion that mediates the cephalic, gastric, and intestinal phases of pancreatic enzyme secretion in response to a meal. 89,90 Rather, the inhibitory effects of vagotomy and anticholinergic drugs on pancreatic enzyme secretion in response to intestinal stimulants are mediated by enteropancreatic reflexes rather than a direct effect on CCK secretion.…”

Section: Vagal Innervationmentioning

confidence: 99%

Regulation of Pancreatic Secretion

Liddle¹

2012

Physiology of the Gastrointestinal Tract

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Control of pancreatic exocrine secretion via muscarinic receptors: Which subtype(s) are involved?

Cited by 13 publications

References 46 publications

Effects of the type of dietary fat on acetylcholine-evoked amylase secretion and calcium mobilization in isolated rat pancreatic acinar cells

Effects of the type of dietary fat on acetylcholine-evoked amylase secretion and calcium mobilization in isolated rat pancreatic acinar cells

Cholinergic Stimulation of Amylase Secretion from Pancreatic Acinar Cells Studied with Muscarinic Acetylcholine Receptor Mutant Mice

Regulation of Pancreatic Secretion

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