Aims: 

Glibenclamide is a sulfonylurea drug that is widely used for the treatment of non-insulin-dependent diabetes mellitus. It was reported that this drug inhibited cystic fibrosis transmembrane regulator (CFTR) Clchannels in epithelial and cardiac cells. Aim of our study was to test whether glibenclamide can inhibit also intracellular chloride channels.

Methods: 

The lipid bilayer technique was used to examine the effects of glibenclamide on the activity of mitochondrial chloride channels. Single channel activity was measured after reconstitution of the mitochondrial membrane vesicles isolated from the rat heart.

Results: 

Conductance of the observed chloride channels was in the range of 90-150 pS and single channel amplitude at 0 mV was 2.6 -3.7 pA (using 250/50 mM KCl cis/trans solutions). Open probability of the chloride channels was in the range of 0.7-0.9. Glibenclamide reversibly inhibited the high chloride channel activity in the concentration range of 100-150 mM in a voltage-dependent manner. The inhibition effect of glibenclamide was pronounced in the presence of 2 mM ATP.

Conclusion: 

Sulfonylurea glibenclamide, blocker of ATP-dependent potassium channel, can also inhibit mitochondrial chloride channels. The obtained results may contribute to understanding mechanisms of its cardiovascular effects: decrease in ischemic preconditioning or anti-arrhythmic effect during the ischemic period.