Abstract
In the canine saphenous vein, inhibitors of cyclo-oxygenase augment contractile responses to acetylcholine, potassium chloride and partial alpha-adrenergic activation. This augmentation is prevented by inhibitors of lipoxygenase, and abolished by calcium entry blockers. These observations suggest that when Ca2+ enters the smooth muscle cells it activates the metabolism of arachidonic acid. If cyclo-oxygenase is inhibited, end-products of lipoxygenase exert a positive feedback on calcium entry. A similar mechanism may explain the hypoxic contractions observed in various blood vessels, including coronary arteries.
MeSH terms
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Acetylcholine / pharmacology
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Animals
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Arachidonic Acid
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Arachidonic Acids / metabolism
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Calcium / physiology*
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Calcium Channel Blockers / pharmacology
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Catechols / pharmacology
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Cyclooxygenase Inhibitors*
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Dogs
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Epinephrine / pharmacology
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Hypoxia / physiopathology
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Indomethacin / pharmacology
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Lipoxygenase Inhibitors*
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Masoprocol
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Muscle Contraction / drug effects
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Muscle, Smooth, Vascular / drug effects*
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Muscle, Smooth, Vascular / physiology
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Potassium / pharmacology
Substances
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Arachidonic Acids
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Calcium Channel Blockers
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Catechols
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Cyclooxygenase Inhibitors
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Lipoxygenase Inhibitors
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Arachidonic Acid
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Masoprocol
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Acetylcholine
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Potassium
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Calcium
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Indomethacin
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Epinephrine