Activation by adrenaline of a low-conductance G protein-dependent K+ channel in mouse pancreatic B cells

Patrik Rorsman, Krister Bokvist, Carina Ämmälä, Per Arkhammar, Per Olof Berggren, Olof Larsson, Karin Wåhlander

Research output: Contribution to journalArticle

105 Scopus citations

Abstract

INSULIN is produced and secreted by the B cells in the endocrine pancreas. In vivo, insulin secretion is under the control of a number of metabolic, neural and hormonal substances. It is now clear that stimulation of insulin release by fuel secretagogues, such as glucose, involves the closure of K+ channels that are sensitive to the intracellular ATP concentration (KATP channels)1. This leads to membrane depolarization and the generation of Ca2+-dependent action potentials2. The mechanisms whereby hormones and neurotransmitters such as adrenaline, galanin and somatostatin, which are released by intraislet nerve endings and the pancreatic D cells, produce inhibition of insulin secretion are not clear3. Here we show adrenaline suppresses B-cell electrical activity (and thus insulin secretion) by a G protein-dependent mechanism, which culminates in the activation of a sulphonylurea-insensitive low-conductance K+ channel distinct from the KATP channel.

Original languageEnglish (US)
Pages (from-to)77-79
Number of pages3
JournalNature
Volume349
Issue number6304
DOIs
StatePublished - Jan 1 1991

ASJC Scopus subject areas

  • General

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