Abstract
Nitric oxide (NO) and prostacyclin (PGI2), formed by NO synthase (NOS) and cyclooxygenase (COX), respectively, are two potent anti-aggregatory vasodilators released from endothelial cells. Both NOS and COX exist as constitutive and inducible isoforms. We have shown that NOS and COX are co-induced in vitro and in vivo by bacterial endotoxin and that low amounts of NO increase whereas high amounts inhibit the activity and expression of inducible COX in vitro.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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6-Ketoprostaglandin F1 alpha / metabolism
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Amino Acid Oxidoreductases / metabolism*
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Animals
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Arginine / analogs & derivatives
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Arginine / pharmacology
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Cell Line
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Endothelium, Vascular / cytology
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Endothelium, Vascular / metabolism
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Endotoxins / toxicity
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Enzyme Induction / drug effects
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Epoprostenol / biosynthesis
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Immunohistochemistry
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Indomethacin / pharmacology
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Macrophages / cytology
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Macrophages / enzymology
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Male
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Mice
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Muscle, Smooth, Vascular / cytology
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Muscle, Smooth, Vascular / enzymology
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Myocardium / enzymology
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Nitric Oxide / antagonists & inhibitors
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Nitric Oxide / biosynthesis
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Nitric Oxide Synthase
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Nitroprusside / pharmacology
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Prostaglandin-Endoperoxide Synthases / metabolism*
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Rats
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Rats, Wistar
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Spleen / enzymology
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omega-N-Methylarginine
Substances
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Endotoxins
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Nitroprusside
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omega-N-Methylarginine
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Nitric Oxide
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6-Ketoprostaglandin F1 alpha
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Arginine
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Epoprostenol
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Nitric Oxide Synthase
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Prostaglandin-Endoperoxide Synthases
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Amino Acid Oxidoreductases
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Indomethacin