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 by 27 ± 6%, but by only 11 ± 3% in diabetic rats (means ± S.E.; P < 0.05). Levcromakalim (1.0 μM) dilated the basilar artery in non-diabetic rats by 45 ± 11%, but by only 20 ± 5% in diabetic rats (P < 0.05). Nitroglycerin (1.0 μM) dilated the basilar artery by 20 ± 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.
- Endothelium-derived hyperpolarizing factor
ASJC Scopus subject areas
- Molecular Biology
- Clinical Neurology
- Developmental Biology