Activation by adrenaline of a low-conductance G protein-dependent K+ channel in mouse pancreatic B cells.
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). This leads to membrane depolarization and the generation of Ca2(+)-dependent action potentials. 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 clear. Here we show that 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.
Rorsman
P
P
Department of Medical Physics, Gothenburg University, Sweden.
Bokvist
K
K
Ammälä
C
C
Arkhammar
P
P
Berggren
P O
PO
Larsson
O
O
Wåhlander
K
K
D000818:Animals; D003000:Clonidine / Q000037:antagonists & inhibitors / Q000494:pharmacology; D004837:Epinephrine / Q000494:pharmacology*; D005947:Glucose / Q000494:pharmacology; D005905:Glyburide / Q000494:pharmacology; D007515:Islets of Langerhans / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D015221:Potassium Channels / Q000187:drug effects*; D014044:Tolbutamide / Q000494:pharmacology; D015016:Yohimbine / Q000494:pharmacology
D015221:Potassium Channels; D015016:Yohimbine; D014044:Tolbutamide; D005947:Glucose; D003000:Clonidine; D005905:Glyburide; D004837:Epinephrine