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.