EFFECT OF DIABETES-MELLITUS ON RESPONSE OF THE BASILAR ARTERY TO ACTIVATION OF ATP-SENSITIVE POTASSIUM CHANNELS

Our goal was to determine whether responses of the basilar artery to a ctivation of ATP-sensitive potassium channels are altered during diabe tes mellitus. We measured changes in diameter of the basilar artery in vivo in non-diabetic and diabetic rats (streptozotocin; 50-60 mg/kg i .p.) in response to activation of ATP-sensitive potassium channels usi ng aprikalim (RP 52891) and levcromakalim (BRL 38227). Aprikalim (1.0 mu M) dilated the basilar artery in non-diabetic rats by 27 +/- 6%, bu t by only 11 +/- 3% in diabetic rats (means +/- S.E.; P < 0.05). Levcr omakalim (1.0 mu M) dilated the basilar artery in non-diabetic rats by 45 +/- 11%, but by only 20 +/- 5% in diabetic rats (P < 0.05). Nitrog lycerin (1.0 mu M) dilated the basilar artery by 20 +/- 5% in non-diab etic rats and 17 +/- 2% in diabetic rats (P > 0.05). Thus, impaired di latation of pial arterioles in diabetic rats in response to aprikalim and levcromakalim is not related to a non-specific effect of diabetes mellitus on vasodilatation. The findings of the present study suggest that ATP-sensitive potassium channels are functional in the rat basila r artery in vivo and are altered during diabetes mellitus.