Muscarinic inhibition of pancreatic B-cells.
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.
Sanchez-Andrés
J V
JV
Department of Physiology, University of Alicante, Spain.
Soria
B
B
D008455:(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride / Q000494:pharmacology; D000818:Animals; D018723:Bethanechol; D001626:Bethanechol Compounds / Q000494:pharmacology; D004594:Electrophysiology; D005947:Glucose / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects* / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects; D016210:Methacholine Chloride / Q000494:pharmacology; D051379:Mice; D010477:Perfusion; D011976:Receptors, Muscarinic / Q000187:drug effects*
D001626:Bethanechol Compounds; D007328:Insulin; D011976:Receptors, Muscarinic; D018723:Bethanechol; D016210:Methacholine Chloride; D008455:(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride; D005947:Glucose