Abstract
Fluoride is a direct activator of G-proteins. In isolated rings of canine coronary artery, fluoride caused relaxation of rings with endothelium, but only slight contraction of rings denuded of endothelium. The endothelium-dependent relaxations to fluoride were inhibited by pertussis toxin, an inhibitor of G-proteins, or by methylene blue, an inhibitor of soluble guanylate cyclase. Therefore, fluoride causes endothelium-dependent relaxations in part by activating a pertussis toxin-sensitive G-protein in the endothelial cells.
MeSH terms
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Acetylcholine / pharmacology
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Aluminum / pharmacology
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Aluminum Chloride
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Aluminum Compounds*
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Animals
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Chlorides / pharmacology
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Coronary Vessels / drug effects
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Dinoprost / pharmacology
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Dogs
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Female
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Fluorides / pharmacology*
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GTP-Binding Proteins / pharmacology
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In Vitro Techniques
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Indomethacin / pharmacology
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Male
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Methylene Blue / pharmacology
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Muscle Contraction / drug effects
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Muscle Relaxation / drug effects
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Muscle, Smooth, Vascular / drug effects
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Nitric Oxide / antagonists & inhibitors*
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Nitroglycerin / pharmacology
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Pertussis Toxin*
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Propranolol / pharmacology
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Virulence Factors, Bordetella / pharmacology*
Substances
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Aluminum Compounds
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Chlorides
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Virulence Factors, Bordetella
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Nitric Oxide
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Aluminum Chloride
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Propranolol
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Dinoprost
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Aluminum
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Pertussis Toxin
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GTP-Binding Proteins
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Nitroglycerin
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Acetylcholine
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Fluorides
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Methylene Blue
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Indomethacin