Influence of glucose on the sodium content of beta-cell-rich pancreatic islets exposed to sulphonamides and amiloride.
Sodium was measured in beta-cell-rich pancreatic islets isolated from ob/ob-mice starved overnight. Exposure to glucose (5 or 20 mmol/l) resulted in about a 30% reduction of the sodium content whether or not the Na+/K+ pump was inhibited by removal of K+. The glucose effect was not potentiated after amiloride depression of Na+/H+ exchange, and it disappeared when combining removal of K+ with the addition of the hyperglycemic sulphonamide diazoxide (400 mumol/l). Tolbutamide (100 mumol/l) counteracted the reduction of sodium obtained with 5 mmol/l glucose both in the presence or absence of extracellular K+. It is concluded that closure of ATP-regulated K+ channels does not necessarily result in a lowering of the sodium content. The pancreatic beta-cells can be regarded as exceptional among the excitable cells in not responding to their natural physiological stimulus (glucose) with increase of sodium.
Wesslén
N
N
Department of Medical Cell Biology, University of Uppsala, Sweden.
Bergsten
P
P
Hellman
B
B
D000255:Adenosine Triphosphate / Q000494:pharmacology; D000584:Amiloride / Q000494:pharmacology*; D000818:Animals; D003981:Diazoxide / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology*; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D051379:Mice; D015221:Potassium Channels / Q000187:drug effects; D012964:Sodium / Q000378:metabolism*; D013449:Sulfonamides / Q000494:pharmacology*; D014044:Tolbutamide / Q000494:pharmacology
D015221:Potassium Channels; D013449:Sulfonamides; D000584:Amiloride; D000255:Adenosine Triphosphate; D014044:Tolbutamide; D012964:Sodium; D005947:Glucose; D003981:Diazoxide