Sulphonamide modulation of sodium content in rat pancreatic islets.
Sodium was measured in rat pancreatic islet exposed to tolbutamide, glipizide, diazoxide or sulfisomidine. When added to a medium with physiologically balanced cations these sulphonamides induced a significant rise of the islet content of sodium. The insulin-releasing compounds, tolbutamide and glipizide, had effects opposite to those of the hyperglycemic diazoxide in counteracting the increase of sodium obtained with removal of K+. The tolbutamide-induced increase in sodium was reversed to a decrease when Ca2+ was omitted from the incubation medium. The increase of sodium, which was also seen with non-hypoglycemic sulphonamides, is itself not sufficient for initiating insulin release. However, it may well represent an important mechanism contributing to the secretory response initiated by Ca2+ entry into the sulfonylurea-depolarized beta-cell.
Ali
L
L
Department of Medical Cell Biology, Biomedicum, Uppsala, Sweden.
Wesslén
N
N
Hellman
B
B
D000818:Animals; D002118:Calcium / Q000494:pharmacology; D003981:Diazoxide / Q000494:pharmacology; D005913:Glipizide / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology; D007515:Islets of Langerhans / Q000378:metabolism*; D008297:Male; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000032:analysis / Q000378:metabolism*; D013449:Sulfonamides / Q000494:pharmacology*; D014044:Tolbutamide / Q000494:pharmacology
D013449:Sulfonamides; D014044:Tolbutamide; D012964:Sodium; D005947:Glucose; D003981:Diazoxide; D011188:Potassium; D002118:Calcium; D005913:Glipizide