Involvement of glibenclamide-sensitive potassium channels in vasorelaxation by cochlear nerve stimulation.

Rabbit aortic rings relaxed with an increase in cyclic guanosine monophosphate and cyclic adenosine monophosphate content in response to exposure to organ fluid of isolated cochleas of the guinea pig following field stimulation (50 Hz, 80 V, 0.2 ms). Relaxations were blocked by 30 microM N(G)-nitro-L-arginine methyl ester added to the vessel rings. This inhibitory effect was reversed by 3 mM L-arginine. Removal of the vascular endothelium also blocked the relaxation response. Glibenclamide attenuated vasorelaxation in a concentration-dependent manner. We conclude that cochlear nerve stimulation induces an endothelium-dependent vasorelaxation involving activation of adenosine triphosphate-sensitive potassium channels.