Pinacidil inhibits insulin release by increasing K+ outflow from pancreatic B-cells

Abstract

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.