Abstract
Endothelium-dependent relaxations in response to substance P and bradykinin were lower in atherosclerotic than in normal human coronary arteries. The relaxation induced by substance P was inhibited by L-NG-monomethylarginine (L-NMMA), which shows that release of nitric oxide is involved in the mediation of endothelium-dependent relaxation in these arteries. L-NMMA also inhibited a basal component of endothelium-dependent relaxation. The basal secretion of nitric oxide was significantly lower in diseased than in normal arteries. These findings suggest that atherosclerotic human coronary arteries lack an important protective mechanism that normally guards against vasospasm and thrombosis.
MeSH terms
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15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
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Adolescent
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Adult
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Arginine / administration & dosage
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Arginine / analogs & derivatives*
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Arginine / pharmacology
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Arteriosclerosis / metabolism*
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Bradykinin / administration & dosage
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Bradykinin / pharmacology
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Child
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Child, Preschool
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Coronary Vessels / drug effects
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Coronary Vessels / metabolism*
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Dose-Response Relationship, Drug
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Drug Synergism
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Endothelium, Vascular / drug effects
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Endothelium, Vascular / metabolism
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Humans
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Middle Aged
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Nitric Oxide / antagonists & inhibitors
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Nitric Oxide / metabolism*
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Prostaglandin Endoperoxides, Synthetic / pharmacology
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Substance P / administration & dosage
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Substance P / antagonists & inhibitors
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Substance P / pharmacology
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Vasoconstriction / drug effects
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Vasodilation / drug effects
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omega-N-Methylarginine
Substances
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Prostaglandin Endoperoxides, Synthetic
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omega-N-Methylarginine
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Nitric Oxide
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Substance P
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15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
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Arginine
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Bradykinin