Abstract
Muscarinic agonists are known to potentiate insulin secretion and increase glucose-induced firing of pancreatic B-cells. Here we report two experimental situations in which inhibitory effects of muscarinic agonists may be observed. (1) Muscarinic agonists delay the onset of the 11.1 mM glucose-induced cell depolarization. (2) At concentrations between 10(-9) and 10(-7) M, acetyl-beta-methylcholine (and also bethanechol and MCN-a-343) decreases cell input resistance and decreases insulin release of islet cells exposed to 5.6 mM glucose.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride / pharmacology
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Animals
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Bethanechol
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Bethanechol Compounds / pharmacology
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Electrophysiology
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Glucose / pharmacology
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Insulin / metabolism*
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Insulin Secretion
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Islets of Langerhans / drug effects*
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Islets of Langerhans / metabolism
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Membrane Potentials / drug effects
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Methacholine Chloride / pharmacology
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Mice
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Perfusion
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Receptors, Muscarinic / drug effects*
Substances
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Bethanechol Compounds
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Insulin
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Receptors, Muscarinic
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Bethanechol
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Methacholine Chloride
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(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride
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Glucose