Alpha2-adrenoreceptor stimulation does not inhibit L-type calcium channels in mouse pancreatic β-cells

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

Research output: Contribution to journalArticle

19 Scopus citations

Abstract

The effects of α2-adrenergic stimulation on the Ca2+-current in mouse pancreatic β-cells were investigated using the patch-clamp technique. When using the conventional whole-cell recording configuration (dialysis of cell interior with pipette solution), addition of adrenaline (1 μM) or the α2-adrenergic agonist clonidine (5 μM) failed to reduce the Ca2+-current, irrespective of whether intracellular GTP (or GTPγ S) was present or not and at both physiological (1.3 mM) and elevated (10.2 mM) Ca2+-concentrations. In fact, in the absence of added guanine nucleotides, the agonists tended to increase the Ca2+-current amplitude in the presence of the higher Ca2+-concentration. Ca2+-channel activation measured at 1.3 mM Ca2+ was not affected by clonidine. Half-maximal activation was observed at ≈-20 mV. In addition, when Ca2+-currents were recorded from intact β-cells, using the perforated patch whole-cell configuration, clonidine (1 μM) also failed to detectably affect the Ca2+-current. It is therefore suggested that the inhibition of β-cell electrical activity and insulin-secretion produced by α2-adrenoreceptor stimulation does not result from suppression of the L-type Ca2+-current.

Original languageEnglish (US)
Pages (from-to)147-157
Number of pages11
JournalBioscience reports
Volume11
Issue number3
DOIs
StatePublished - Jun 1 1991

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Keywords

  • adrenaline
  • Ca-current
  • insulin
  • pancreatic β-cell

ASJC Scopus subject areas

  • Cell Biology
  • Biochemistry, Genetics and Molecular Biology(all)

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