Effect of diabetes mellitus on response of the basilar artery to activation of ATP-sensitive potassium channels

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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 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.

Original languageEnglish (US)
Pages (from-to)35-39
Number of pages5
JournalBrain Research
Volume636
Issue number1
DOIs
StatePublished - Feb 4 1994

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KATP Channels
Basilar Artery
Diabetes Mellitus
Cromakalim
Nitroglycerin
Arterioles
Streptozocin
Vasodilation
Dilatation
aprikalim

Keywords

  • Aprikalim
  • Endothelium-derived hyperpolarizing factor
  • Levcromakalim
  • Nitroglycerin
  • Rat

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

Cite this

Effect of diabetes mellitus on response of the basilar artery to activation of ATP-sensitive potassium channels. / Mayhan, William G.

In: Brain Research, Vol. 636, No. 1, 04.02.1994, p. 35-39.

Research output: Contribution to journalArticle

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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 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.",
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