Imidazolines and pancreatic hormone secretion

Ann N Y Acad Sci. 1999 Jun 21:881:217-28. doi: 10.1111/j.1749-6632.1999.tb09364.x.

Abstract

A range of imidazoline derivatives are known to be effective stimulators of insulin secretion, and this response correlates with closure of ATP-sensitive potassium channels in the pancreatic beta-cell. However, mounting evidence indicates that potassium channel blockade may form only part of the mechanism by which imidazolines exert their effects on insulin secretion. Additionally, it remains unclear whether members of this class of drugs can bind directly to potassium channel components and whether occupation of a single binding site accounts for their functional activity. This review considers recent developments in the field and highlights evidence that does not fit readily with the concept that a single mechanism of action is sufficient to mediate the effects of imidazolines on pancreatic hormone secretion.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Binding Sites
  • Humans
  • Imidazoles / pharmacokinetics
  • Imidazoles / pharmacology*
  • Imidazoline Receptors
  • Insulin / metabolism
  • Insulin Secretion
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / metabolism*
  • Potassium Channels / physiology
  • Receptors, Drug / physiology*

Substances

  • Imidazoles
  • Imidazoline Receptors
  • Insulin
  • Potassium Channels
  • Receptors, Drug