Activation, but not inhibition, by glucose of Ca2+-dependent K+ permeability in the rat pancreatic B-cell.
The effect of glucose on the Ca2+-activated K+ permeability in pancreatic islet cells was investigated by measuring the rate of 86Rb efflux, 45Ca efflux and insulin release from perifused rat pancreatic islets exposed to step-wise increased in glucose concentration. When the glucose concentration was raised from intermediate (8.3 or 11.1 mM) to higher values, a rapid and sustained increase in 86Rb outflow, 45Ca outflow and insulin release was observed. Likewise, in the presence of 8.3 or 16.7 mM glucose, tolbutamide increased 86Rb and 45Ca efflux, as well as insulin release. In the two series of experiments, a tight correlation was found between the magnitude of the changes in 86Rb and 45Ca outflow, respectively. It is concluded that, at variance with current ideas, glucose does not inhibit the response to cytosolic Ca2+ of the Ca2+-sensitive modality of K+ extrusion. On the contrary, as a result of its effect upon Ca2+ handling, glucose stimulates the Ca2+-activated K+ permeability.
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology*; D005947:Glucose / Q000494:pharmacology*; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D012413:Rubidium / Q000378:metabolism
D005947:Glucose; D012413:Rubidium; D011188:Potassium; D002118:Calcium