Recently, we reported that restraint stress-induced elevation of plasma levels of adrenaline, but not of noradrenaline, was suppressed by intravenous and intracerebroventricular (i.c.v.) administration of glucose via brain thromboxane A₂-dependent mechanisms. (Yamaguchi et al., 2022). Since glucose can be converted to ATP in the brain cells, in the present study, we investigate whether ATP-sensitive K⁺ channel (K_ATP channel) activity in the brain is involved in changes of plasma levels of catecholamines in urethane anesthetized rats. I.c.v. administered diazoxide (20 µg/rat), a K_ATP channel opener, and A-769662 (25 µg/rat), an AMPK activator, elevated plasma levels of adrenaline, but not noradrenaline. In contrast, i.c.v administered glibenclamide (25 µg/rat), a K_ATP channel antagonist, did not alter plasma levels of adrenaline. I.c.v. pretreatment with SQ29548 (10 µg/rat), a thromboxane A₂ receptor antagonist, attenuated diazoxide- and A-7969662-induced elevation of plasma levels of adrenaline. These results suggest that K_ATP channel activation in the brain might trigger the activation of thromboxane A₂ receptor, resulting in elevation of plasma levels of adrenaline.