Pinacidil inhibits insulin release by increasing K+ outflow from pancreatic B-cells.
Pinacidil, a putative K+ channel opener, increased 86Rb outflow from rat pancreatic islets perifused in the presence of glucose, 2-ketoisocaproate or tolbutamide. Furthermore, the drug markedly inhibited 45Ca outflow and insulin release from glucose-stimulated islets. These results represent the first indication of an effect of pinacidil on ionic and secretory events in endocrine cells. Indirect findings suggest that, in pancreatic islet cells, pinacidil could affect ATP-sensitive K+ channels.
Lebrun
P
P
Laboratory of Pharmacology, Brussels Free University School of Medicine, Belgium.
Devreux
V
V
Hermann
M
M
Herchuelz
A
A
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D006146:Guanidines / Q000494:pharmacology*; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D020110:Pinacidil; D011188:Potassium / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects; D051381:Rats
D006146:Guanidines; D007328:Insulin; D015221:Potassium Channels; D020110:Pinacidil; D000255:Adenosine Triphosphate; D011188:Potassium