Blockade of K(ATP) channels with glibenclamide does not alter functional activation of cerebral blood flow in the unanesthetized rat.

Possible involvement of ATP-sensitive K(+) (K(ATP)) channels in the cerebral blood flow (CBF) response to neuronal functional activation was investigated in unanesthetized rats. Glibenclamide (1, 2, or 10 micromol/l), a specific inhibitor of K(ATP) channels, was infused intracisternally continuously for 30 min prior to and during the 1-min period of measurement of CBF. Unilateral functional activation was maintained throughout the measurement of CBF by continuous stroking of the vibrissae on the left side of the face. Local CBF was determined bilaterally by the quantitative autoradiographic [14C]iodoantipyrine method in four structures of the whisker-to-barrel cortex pathway and in 18 structures unrelated to the pathway. Glibenclamide tended to lower baseline CBF in almost all regions examined, statistically significantly (P<0.05) in the cerebellar lobules with all doses, in the cerebellar cortex with 10 micromol/l, in the pontine nuclei with 2 and 10 micromol/l, and in the spinal trigeminal nucleus of the unstimulated side with all doses. Vibrissal stimulation increased CBF unilaterally in all the stations of the pathway, but the percent increases were not statistically significantly affected by the glibenclamide treatment, except in the spinal trigeminal nucleus where it was reduced statistically significantly (P<0.05) only by 2 micromol/l glibenclamide. These results indicate that K(ATP) channels may play a role in the tonic regulation of baseline CBF in some regions but provide no support for their role in the increases in CBF evoked by functional activation.