Dexamethasone enhances adenosine 5′-triphosphate-sensitive potassium channel expression in the blood-brain tumor barrier in a rat brain tumor model

This study was performed to determine whether dexamethasone (DEX) had an effect on ATP-sensitive potassium channels (KATP channels) in blood-brain tumor barrier (BTB). Using a rat brain glioma model, we found that DEX could significantly increase the expression of KATP channels protein at tumor sites. And bradykinin-induced increase of KATP channels protein was further enhanced after DEX pretreatment for 3 consecutive days via Western blots and immunohistochemistry methods. In addition, DEX pretreatment enhanced bradykinin-mediated increase of the density of IKATP in the cultured rat C6 glioma cells using the patch-clamp technique in a whole-cell configuration. DEX significantly decreased the BTB permeability, but it did not reduce bradykinin-mediated BTB permeability increase, which were significantly attenuated by the KATP channel antagonist glibenclamide. This led to the conclusion that DEX-mediated change in BTB permeability is, at least partly, due to accelerated formation of KATP channel, an important target in the biochemical regulation of this process.