The K-ATP channel regulates the effect of Ca2+ on gap junction permeability in cultured astrocytes.

Using the scrape-loading technique we show that tolbutamide and glybenzcyclamide, two inhibitors of the K+ channel sensitive to ATP (K-ATP channel), partially prevent the inhibition of gap junction permeability promoted by Ca2+ in cultured astrocytes. This effect was dose-dependent, reaching a maximum at 400 microM and 1 microM of tolbutamide and glybenzcyclamide, respectively. The presence of the Ca2+ ionophore A-23187 strongly reduced the concentration of Ca2+ required to block gap junction permeability but did not abolish the effect of tolbutamide and glybenzcyclamide. These results suggest that the effect of these two compounds are not brought about by control of the intracellular concentration of Ca2+ but probably by the promotion of plasma membrane depolarization.