Modulation of rat pancreatic amylase secretion and muscarinic receptor populations by chronic bethanechol treatment

Larose, Louise; Poirier, Guy G.; Dumont, Yvan; Frégeau, Chantal J.; Blanchard, Louise M.; Morisset, Jean

doi:10.1016/0014-2999(83)90637-4

Cited by 24 publications

(9 citation statements)

References 36 publications

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“…The present study and other reports have clarified that muscarinic receptors are indeed present on rat pancreatic acini (19,20 (29,30). The linearity of the Scatchard plot of [3H]QNB binding to isolated pancreat ic acini is considered to be evidence for the presence of a single class of binding sites.…”

Section: Discussionsupporting

confidence: 77%

Release of Digestive Enzymes from Isolated Rat Pancreatic Acini Following Muscarinic Stimulation:A Comparative Study with Enzyme Release and Receptor Binding.

et al. 1991

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ABSTRACT-Effect of cholinergic stimulation on the release of digestive enzymes from isolated rat pancreatic acini prepared by collagenase digestion was investigated. The release of enzymes (amylase, chymotrypsinogen, lipase) increased linearly with the time of incubation in the absence of secretagogues. Carbachol, a muscarinic ago nist, induced a remarkable increase in the release of these enzymes. This carbachol stimulated amylase release showed a biphasic curve, and its maximal response was observed at 10-5 M. The release patterns of chymotrypsinogen and lipase were similar to that of amylase. This carbachol-stimulated amylase release was inhibited by atro pine in a dose-dependent manner, with an ED50 value of 1.17 X 10-8 M. Other cho linergic agonists such as methacholine also stimulated the release of these enzymes, and these increases in the release were inhibited by atropine. [2,3-b1[1,4]-benzodiazepine-6-one), on pancreatic acini was also investigated. Based on these results, it has been concluded that isolated rat pancreatic acini have muscarinic receptors and are useful for analyzing the mecha nism of pancreatic enzyme secretion.Pancreatic exocrine secretion is regulated by neural and humoral factors (1-3). Recent de velopment in the techniques to isolate pan creatic acinar cells such as enzyme digestion, chelation and mechanical shearing procedures (2, 4, 5) have facilitated the pharmacological analyses of such regulatory mechanisms on pancreatic exocrine secretion. In fact, pan creatic physiological functions including the re sponsiveness of enzyme secretion to various secretagogues and receptors coupled with pan creatic exocrine function has been clarified (6-9). Amylase secretion has been used as an index for pancreatic exocrine function and for

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Section: Discussionsupporting

confidence: 77%

Release of Digestive Enzymes from Isolated Rat Pancreatic Acini Following Muscarinic Stimulation:A Comparative Study with Enzyme Release and Receptor Binding.

et al. 1991

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“…However, our re sults differ from those of other studies using dispersed pancreatic acini [3][4][5]. In a pre vious study by Asselin et al [5] using dis persed acini from rat pancreas, first incubat ing acini with carbachol not only caused a 40% down-regulation of the high affinity muscarinic, cholinergic receptors but also caused 30% up-regulation of the low affinity muscarinic, cholinergic receptors with no re sultant change in the total number of musca rinic, cholinergic receptors.…”

Section: Discussioncontrasting

confidence: 56%

“…In particular, because previous investiga tions have established that pancreatic acinar cells possess multiple classes of muscarinic cholinergic receptors [3,4,[6][7][8], we have examined the relationship between the ability of carbachol to occupy the various classes of cholinergic receptors and the accompanying down-regulation of secretagogue receptors. 0.5 M KHjPO, (pH 7.4), [Tyrilbombesin (6 pg in 6 pi of HiO) and N al25I (1 mCi) were added and the mix ture was incubated at 4 °C for 6 min.…”

Section: Introductionmentioning

confidence: 99%

Carbachol-Induced Down-Regulation of Receptors for Pancreatic Secretagogues

Vinayek

Murakami²,

Sharp³

et al. 1990

Digestion

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Pancreatic acini possess a high affinity class of cholinergic receptors and a low affinity class of cholinergic receptors. Carbachol occupation of high affinity cholinergic receptors produces a reduction in binding of [³H]N-methylscopolamine. First incubating acini with carbachol caused a complete loss of high affinity cholinergic receptors with no change in the number or affinity of low affinity cholinergic receptors. Carbachol occupation of low affinity cholinergic receptors appears to produce a reduction in binding of ¹²⁵I-CCK-8 and ¹²⁵I-[Tyr⁴]bombesin. Acini possess two classes of CCK receptors. One class has a high affinity for CCK-8; the other class has a low affinity for CCK-8. First incubating acini with carbachol caused a 60% decrease in the number of high affinity CCK receptors with no change in the number of low affinity receptors or the affinities of either class of receptors for CCK-8. Acini possess a single class of bombesin receptors and first incubating acini with carbachol caused a 40% decrease in the number of bombesin receptors with no change in their affinity for bombesin.

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“…Acini were exposed to both stimuli for 30 min at 37 °C. At the end of the incubation period in the presence (stimulated) or in the absence (basal) of secretagogues, amy lase release from pancreatic acini was determined as previously described by Larose et al [ 12]. Amylase activity was evaluated by the method of Ceska et al [13] using phadebas blue starch reagent as reported by Gardner et al [ 14], Amylase release was expressed as the percentage of initial amylase activity present in the acini released into the medium during 30 min at 37 °C minus basal release giving net amylase release.…”

Section: Anim Al Model Male Sprague-dawlely Rats (250-260 G) From Thementioning

confidence: 99%

Alterations of the Pancreatic Secretory Responses to Secretin and to the lonophore A23187 by Reserpine: A Calcium-Mediated Phenomenon?

Benrezzak¹,

Bérubé²,

St-Jean³

et al. 1994

Digestion

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This study was undertaken to further characterize the secretory response of the rat pancreas after reserpine treatment. Rats were given reserpine (1 mg kg^-1 day^-1 i.p.) or vehicle for 7 days. To distinguish between specific effects of reserpine and those related to secondary malnutrition caused by the drug, the secretory response of a group of pair-fed (PF) animals to reserpine was also investigated. Amylase release from dispersed pancreatic acini, prepared from control (C), PF and reserpine-treated (R) rats were used to evaluate functional secretory capacity. Reserpine and pair-feeding caused reduced responses of pancreatic acini to secretin. The pair-feeding-altered secretin response was greatly improved by increasing extracellular Ca²⁺ concentration, whereas a slight improvement was noticed in the R group. Reserpine significantly reduced the secretory response to the ionophore A23187 at concentrations above 5 × 10^-7M in 1.25 mM Ca²⁺; in 2.5 mM Ca²⁺, the response to the ionophore was significantly higher in the R group than in C at all ionophore concentrations. Furthermore, at 2 × 10^-7M ionophore, the secretory response to secretin in the R group became significantly higher than that in the C group but comparable to that of the control + ionophore. In conclusion, reserpine affects the secretory response to secretin as did pre-exposure of pancreatic acini to a high concentration of carbamylcholine. The modified secretory response to the ionophore following reserpine treatment indicates that reserpine may act as a ‘Ca²⁺ entry mechanism’ antagonist which may explain the partial reduction in the secretin response.

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Modulation of rat pancreatic amylase secretion and muscarinic receptor populations by chronic bethanechol treatment

Cited by 24 publications

References 36 publications

Release of Digestive Enzymes from Isolated Rat Pancreatic Acini Following Muscarinic Stimulation:A Comparative Study with Enzyme Release and Receptor Binding.

Release of Digestive Enzymes from Isolated Rat Pancreatic Acini Following Muscarinic Stimulation:A Comparative Study with Enzyme Release and Receptor Binding.

Carbachol-Induced Down-Regulation of Receptors for Pancreatic Secretagogues

Alterations of the Pancreatic Secretory Responses to Secretin and to the lonophore A23187 by Reserpine: A Calcium-Mediated Phenomenon?

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