Abstract
The role of the neuronal isoform of the nitric oxide (NO) synthase (nNOS) in the regulation of the cerebrovascular tone was studied in vitro. Selective inhibition of nNOS by 7-nitro indazole monosodium salt (7-NINA) failed to alter the resting tension and the relaxant effect of bradykinin in isolated rat middle cerebral arteries. These results indicate that 1./ 7-NINA is selective for nNOS and 2./ cerebrovascular nNOS is involved neither in the resting NO production nor in the mediation of the relaxant effect of bradykinin. Therefore, nNOS-derived NO that contributes to the maintenance of the resting cerebral blood flow in vivo appears to be released from neurons and/or glial cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Bradykinin / pharmacology*
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Endothelium, Vascular / drug effects
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Endothelium, Vascular / enzymology
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Enzyme Inhibitors / pharmacology*
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In Vitro Techniques
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Indazoles / pharmacology*
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Male
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Middle Cerebral Artery / drug effects*
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Middle Cerebral Artery / enzymology
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Muscle Tonus / drug effects
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Muscle, Smooth, Vascular / drug effects*
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Muscle, Smooth, Vascular / enzymology
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Nitric Oxide Synthase / antagonists & inhibitors*
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Nitric Oxide Synthase Type I
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Rats
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Rats, Wistar
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Uridine Triphosphate / pharmacology
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Vasoconstriction / drug effects
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Vasodilation / drug effects
Substances
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Enzyme Inhibitors
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Indazoles
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Nitric Oxide Synthase
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Nitric Oxide Synthase Type I
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Nos1 protein, rat
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Bradykinin
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Uridine Triphosphate
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7-nitroindazole