3H-methyl scopolamine binding to dispersed pancreatic acini

Appert, Hubert E.; Chiu, Ted H.; Budd, G. C.; Leonardi, Anthony; Howard, John M.

doi:10.1007/bf00210454

Cited by 14 publications

(5 citation statements)

References 25 publications

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“…The affinity and B, , , of NMS to the muscarinic receptors in the pancreatic plasma membranes of normal rats as well as the non-specific binding are in accordance with the results reported earlier (Appert et al 1981;Dehaye et al 1984;Louie & Owyang 1986).…”

Section: Discussionsupporting

confidence: 91%

Decrease in the Number of Muscarinic Receptors in Rat Pancreas after Chronic Alcohol Intake

Grönroos

Kaila

Aho

et al. 1989

Pharmacology & Toxicology

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The effect of eight months of alcohol intake on the number and affinity of muscarinic receptor sites in the rat pancreatic tissue were measured by using N-3H-methylscopolamine (NMS) as a radioligand. There were no differences in the receptor affinities for NMS between the alcohol-exposed and age-matched control animals, but the number of muscarinic receptor sites was 60 percent lower in the alcoholic animals. The present experimental model is consistent with altered food and water intake as consequences of chronic alcoholism and thus changes in food and water consumption may participate in mediating the effects of chronic alcohol intake on NMS binding sites. We suggest that the previously reported marked alcohol-induced increase in pancreatic acetylcholine levels, which has been proposed to play a crucial role in the pathogenesis of acute alcoholic pancreatitis, may be a secondary phenomenon induced by increased resistance at the muscarinic receptor level.

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Section: Discussionsupporting

confidence: 91%

Decrease in the Number of Muscarinic Receptors in Rat Pancreas after Chronic Alcohol Intake

Grönroos

Kaila

Aho

et al. 1989

Pharmacology & Toxicology

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“…[3H]myoinositol (30 ,Ci/ml) for 2 h. The acini were pelleted by centrifugation at 11,000 g for 10 s. The pellet was placed into 5 ml of ice-cold chloroform-methanol (2:1) and extracted against 5 ml of I N HCI. An additional 5 ml ofchloroform was added and the organic layer was washed twice with cold I N HCl.…”

Section: Methodsmentioning

confidence: 99%

Diminished agonist-stimulated inositol trisphosphate generation blocks stimulus-secretion coupling in mouse pancreatic acini during diet-induced experimental pancreatitis.

Powers¹,

Saluja²,

Houlihan³

et al. 1986

J. Clin. Invest.

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Young female mice fed a choline-deficient, ethionine-supplemented (CDE) diet rapidly develop acute hemorrhagic pancreatitis. We have observed that pancreatic acini prepared from these mice are unable to secrete amylase in response to addition of the cholinergic agonist carbachol, although they retain the ability to secrete amylase in response to the Ca2+ ionophore A23187. The CDE diet does not alter the binding characteristics (Kd or the maximal number of binding sites) for muscarinic cholinergic receptors as tested using the antagonist jHIN-methylscopolamine nor the competition for this binding by carbachol. Addition of carbachol to acini prepared from mice fed the CDE diet does not result in as marked an increase in cytosolic free Ca2+ levels as that noted in control samples (evaluated using quin2 fluorescence). These observations indicate that the CDE diet interferes with stimulus-secretion coupling in mouse pancreatic acini at a step subsequent to hormone-receptor binding and prior to Ca2`release. This conclusion is confirmed by our finding that the hormone-stimulated generation of IHiinositol phosphates (inositol trisphosphate, inositol bisphosphate, and inositol monophosphate) from acini labeled with VfHlmyoinositol is markedly reduced in acini prepared from mice fed the CDE diet. This reduction is not due to a decrease in phosphatidylinositol4,5-bisphosphate. This communication represents the first report of a system in which a blockade of inositol phosphate generation can be related to a physiologic defect and pathologic lesion.

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“…The observation that the affinity of muscarinic receptors dou bled in regenerating cells was compatible with the fact that the dose-response curves of amylase release in both percent of the total and per cell stimulated by carbamylcholine shifted to the left in comparison with the other groups. It has been reported that there are high-and low-affinity muscarinic recep tors on rat pancreatic acinar cells and that high-affinity receptors are related to amylase secretion [1][2][3]. In regenerating acinar cells, the apparent affinity might increase because some of the low-affinity receptors may change into high-affinity ones.…”

Section: Discussionmentioning

confidence: 99%

“…Muscarinic receptors of acinar cells have been studied by binding assay using radiolabeled ligands [1][2][3]. Dumont et al [4] showed that muscarinic receptors of pan creatic acinar cells have a higher affinity in 5-day-old rats than in 11-day-old or ma ture rats.…”

Section: Introductionmentioning

confidence: 99%

Changes in Muscarinic Receptors and Amylase Secretion in Regenerating Acinar Cells of Rat Pancreas

Sumii

Kimura²,

Ogami³

et al. 1988

Digestion

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Atrophic pancreatic acinar cells of copper-deficient rats recovered after copper supplementation. To clarify whether the recovered cells are regenerative and amylase secretion via muscarinic receptors alters, [³H]-thymidine uptake, [³H]-quinuclidinyl benzilate binding and amylase release were studied in these rats and compared with the values of 5-day-old and 21-week-old rats. The [³H]-thymidine uptake study indicated that the recovered acinar cells were regenerative. The number of muscarinic receptors in regenerating cells was equal to that in mature cells and was one third that in cells of 5-day-old rats. The apparent dissociation constant of muscarinic receptors was about 0.73 × 10^-10M for the regenerating cells, 0.65 × 10^-10M for 5-day-old rats, and 1.70 × 10^-10M for 21-week-old rats. Amylase release, as a percent of total amylase, was maintained relatively steady in spite of the low amylase content in regenerating cells. These observations suggest that the affinity of muscarinic receptors increases to compensate the impaired amylase synthesis in regenerating acinar cells and that their amylase secretion via muscarinic receptors is different from that in 5-day-old or mature rats.

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3H-methyl scopolamine binding to dispersed pancreatic acini

Cited by 14 publications

References 25 publications

Decrease in the Number of Muscarinic Receptors in Rat Pancreas after Chronic Alcohol Intake

Decrease in the Number of Muscarinic Receptors in Rat Pancreas after Chronic Alcohol Intake

Diminished agonist-stimulated inositol trisphosphate generation blocks stimulus-secretion coupling in mouse pancreatic acini during diet-induced experimental pancreatitis.

Changes in Muscarinic Receptors and Amylase Secretion in Regenerating Acinar Cells of Rat Pancreas

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