POSSIBLE INVOLVEMENT OF ATP-SENSITIVE K+ CHANNELS IN THE INHIBITION OF RAT CENTRAL ADRENERGIC NEUROTRANSMISSION UNDER HYPOXIA

By using rat brain cortical slices preloaded with [H-3]norepinephrine, we examined whether ATP-sensitive K+ channels are involved in altered adrenergic neurotransmission during hypoxia. The tritium overflow evo ked by transmural nerve stimulation (TNS) was significantly inhibited at 5 min of hypoxia and reached the maximum inhibition at 20 min. The inhibition of the TNS-evoked tritium overflow under a 20-min hypoxia w as reversed by subsequent reoxygenation and was concentration-dependen tly antagonized by glibenclamide (0.1 and 1 muM). Rb-86+ efflux was in creased after introduction of hypoxia and reached the peak value at ab out 20 min, which was concentration-dependently antagonized by glibenc lamide (0.1 - 10 muM). Hypoxia decreased cortical ATP content. Linear correlations were mutually observed among the changes by hypoxia in th e TNS-evoked tritium overflow, tissue ATP content and Rb-86+ efflux. T he spontaneous tritium outflow was inhibited only after hypoxic period s of more than 16 min, the inhibition being reversed by reoxygenation and antagonized by 1 muM glibenclamide. These results suggest that the inhibition of rat central adrenergic neurotransmission during hypoxia may be associated with an activation of ATP-sensitive K+ channels.