Abstract
The goal of this study was to test the hypothesis that administration of superoxide dismutase restores nitric oxide synthase-mediated dilatation of the basilar artery during diabetes mellitus. We measured the diameter of the basilar artery in vivo in nondiabetic and diabetic rats (streptozotocin; 50-60 mg/kg i.p.) in response to nitric oxide synthase-dependent agonists (acetylcholine and bradykinin) and a nitric oxide synthase-independent agonist (nitroglycerin) before and during application of superoxide dismutase. Topical application of acetylcholine (1.0 and 10 μM) and bradykinin (1.0 and 10 μM) produced dose-related dilatation of the basilar artery in nondiabetic and diabetic rats. However, the magnitude of vasodilation produced by acetylcholine and bradykinin was significantly less in diabetic rats. Topical application of nitroglycerin (0.1 and 1.0 μM) produced similar dose-related dilatation of the basilar artery in nondiabetic and diabetic rats. Treatment with superoxide dismutase (150 U/ml) did not alter baseline diameter of the basilar artery in nondiabetic and diabetic rats. However, topical application of superoxide dismutase partially restored nitric oxide synthase-dependent dilatation of the basilar artery in diabetic rats towards that observed in nondiabetic rats. Superoxide dismutase did not alter dilatation of the basilar artery in nondiabetic rats. These findings suggest that impaired nitric oxide synthase-dependent dilatation of the basilar artery during diabetes mellitus may be related, in part, to enhanced release of oxygen-derived free radicals.
Original language | English (US) |
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Pages (from-to) | 204-209 |
Number of pages | 6 |
Journal | Brain Research |
Volume | 760 |
Issue number | 1-2 |
DOIs | |
State | Published - Jun 20 1997 |
Keywords
- Acetylcholine
- Bradykinin
- Brain
- Nitric oxide
- Nitroglycerin
- Oxygen radical
- Rat
- Superoxide anion
ASJC Scopus subject areas
- General Neuroscience
- Molecular Biology
- Clinical Neurology
- Developmental Biology