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Thiopental inhibits K+ permeability of rat and mouse pancreatic beta-cells.

The effects of thiopental on the insulin release and 86Rb efflux from isolated rat islets and on parameters of the electrical activity of single beta-cells of mice were studied. Thiopental 0.2 and 1.0 mM increased by 16.6 and 33.3%, respectively, the insulin release induced by 6.0 mM glucose. Thiopental reduced the 86Rb efflux rate in both 0 and 6.0 mM glucose, but had only a slight effect in 16.7 mM glucose. Menadione (20 microM) did not block the inhibitory effect of thiopental on 86Rb efflux. Thiopental induced a reversible membrane depolarization in a dose-dependent manner (0.2-1.0 mM). It also induced electrical activity at a subthreshold glucose concentration and continuous spiking in presence of 11.1 mM glucose. In the presence of 2,4-dinitrophenol (20 microM) this continuous spiking was changed to an oscillatory activity similar to that induced by 11.1 mM glucose. Thiopental (0.5 mM) induced an increase in input resistance of 12.7, 17.9 and 16.0% in 0, 5.6 and 11.1 mM glucose, respectively. The thiopental-induced changes in insulin secretion, 86Rb efflux and electrical parameters indicate that K+ permeability was affected in both rat and mouse beta-cells. Our results suggest that thiopental is a direct inhibitor of the glucose-sensitive K+ permeability in the beta-cell.