Abstract
Our goal was to determine whether responses of the basilar artery to activation of ATP-sensitive potassium channels are altered during diabetes 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 using aprikalim (RP 52891) and levcromakalim (BRL 38227). Aprikalim (1.0 μM) dilated the basilar artery in non-diabetic rats by27 ± 6%, but by only11 ±3% in diabetic rats (means±S.E.; P< 0.05). Levcromakalim (1.0 μM) dilated the basilar artery in non-diabetic rats by45 ± 11%, but by only20 ± 5% in diabetic rats ( P < 0.05). Nitroglycerin (1.0 μM) dilated the basilar artery by20 ± 5% in non-diabetic rats and 17 ± 2% in diabetic rats ( P < 0.05). Thus, impaired dilatation 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 basilar artery in vivo and are altered during diabetes mellitus.
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