Muscarinic inhibition of pancreatic B-cells

Eur J Pharmacol. 1991 Nov 19;205(1):88-91.

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

  • Research Support, Non-U.S. Gov't

MeSH terms

  • (4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride / pharmacology
  • Animals
  • Bethanechol
  • Bethanechol Compounds / pharmacology
  • Electrophysiology
  • Glucose / pharmacology
  • Insulin / metabolism*
  • Insulin Secretion
  • Islets of Langerhans / drug effects*
  • Islets of Langerhans / metabolism
  • Membrane Potentials / drug effects
  • Methacholine Chloride / pharmacology
  • Mice
  • Perfusion
  • Receptors, Muscarinic / drug effects*

Substances

  • Bethanechol Compounds
  • Insulin
  • Receptors, Muscarinic
  • Bethanechol
  • Methacholine Chloride
  • (4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride
  • Glucose