Catecholamine inhibition of Ca2+-induced insulin secretion from electrically permeabilised islets of Langerhans

FEBS Lett. 1987 Jul 13;219(1):139-44. doi: 10.1016/0014-5793(87)81206-1.

Abstract

Noradrenaline (1-10 microM) inhibited Ca2+-induced insulin secretion from electrically permeabilised islets of Langerhans with an efficacy similar to that for inhibition of glucose-induced insulin secretion from intact islets. The inhibition of insulin secretion from permeabilised islets was blocked by the alpha 2-adrenoreceptor antagonist, yohimbine. Adenosine 3',5'-cyclic monophosphate (cAMP) did not relieve the noradrenaline inhibition of Ca2+-induced secretion from the permeabilised islets, although noradrenaline did not affect the secretory responses to cAMP at substimulatory (50 nM) concentrations of Ca2+. These results suggest that catecholamines do not inhibit insulin secretion solely by reducing B-cell adenylate cyclase activity, and imply that one site of action of noradrenaline is at a late stage in the secretory process.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bucladesine / antagonists & inhibitors
  • Calcium / antagonists & inhibitors*
  • Catecholamines / pharmacology*
  • Cyclic AMP / antagonists & inhibitors
  • Electric Stimulation
  • Glucose / antagonists & inhibitors
  • In Vitro Techniques
  • Insulin / metabolism*
  • Insulin Secretion
  • Islets of Langerhans / drug effects*
  • Islets of Langerhans / metabolism
  • Norepinephrine / antagonists & inhibitors
  • Norepinephrine / pharmacology
  • Permeability
  • Rats
  • Yohimbine / pharmacology

Substances

  • Catecholamines
  • Insulin
  • Yohimbine
  • Bucladesine
  • Cyclic AMP
  • Glucose
  • Calcium
  • Norepinephrine