Anti-inflammatory glucocorticoids inhibit the induction by endotoxin of nitric oxide synthase in the lung, liver and aorta of the rat

The induction by endotoxin of Ca 2+-independent nitric oxide (NO) synthase in the lung and liver of the rat was prevented by the glucocorticoids dexamethasone and cortisol but not by progesterone. The activity of the constitutive Ca 2+-dependent NO synthase in the brain and the aorta was not affecte...

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Veröffentlicht in:Biochemical and biophysical research communications 1990-11, Vol.172 (3), p.1042-1048
Hauptverfasser: Knowles, R.G., Salter, M., Brooks, S.L., Moncada, S.
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container_end_page 1048
container_issue 3
container_start_page 1042
container_title Biochemical and biophysical research communications
container_volume 172
creator Knowles, R.G.
Salter, M.
Brooks, S.L.
Moncada, S.
description The induction by endotoxin of Ca 2+-independent nitric oxide (NO) synthase in the lung and liver of the rat was prevented by the glucocorticoids dexamethasone and cortisol but not by progesterone. The activity of the constitutive Ca 2+-dependent NO synthase in the brain and the aorta was not affected by treatment with either endotoxin or glucocorticoids. In the aorta a Ca 2+-independent NO synthase was also found following endotoxin treatment of rats, and this induction was likewise prevented by dexamethasone. The Ca 2+-dependent NO synthase in the aorta was located in the vascular endothelium, whereas the Ca 2+-independent enzyme was predominantly located in the vascular smooth muscle layer. Inhibition of induction of the Ca 2+-independent NO synthase in vivo may underlie some of the physiological and pharmacological effects of the anti-inflammatory glucocorticoids.
doi_str_mv 10.1016/0006-291X(90)91551-3
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The activity of the constitutive Ca 2+-dependent NO synthase in the brain and the aorta was not affected by treatment with either endotoxin or glucocorticoids. In the aorta a Ca 2+-independent NO synthase was also found following endotoxin treatment of rats, and this induction was likewise prevented by dexamethasone. The Ca 2+-dependent NO synthase in the aorta was located in the vascular endothelium, whereas the Ca 2+-independent enzyme was predominantly located in the vascular smooth muscle layer. 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The activity of the constitutive Ca 2+-dependent NO synthase in the brain and the aorta was not affected by treatment with either endotoxin or glucocorticoids. In the aorta a Ca 2+-independent NO synthase was also found following endotoxin treatment of rats, and this induction was likewise prevented by dexamethasone. The Ca 2+-dependent NO synthase in the aorta was located in the vascular endothelium, whereas the Ca 2+-independent enzyme was predominantly located in the vascular smooth muscle layer. Inhibition of induction of the Ca 2+-independent NO synthase in vivo may underlie some of the physiological and pharmacological effects of the anti-inflammatory glucocorticoids.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>1700903</pmid><doi>10.1016/0006-291X(90)91551-3</doi><tpages>7</tpages></addata></record>
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subjects Amino Acid Oxidoreductases - biosynthesis
Animals
Anti-Inflammatory Agents - pharmacology
Aorta - drug effects
Aorta - enzymology
Dexamethasone - pharmacology
Endotoxins - pharmacology
Enzyme Induction - drug effects
Glucocorticoids - pharmacology
Hydrocortisone - pharmacology
Liver - drug effects
Liver - enzymology
Lung - drug effects
Lung - enzymology
Male
Nitric Oxide Synthase
Progesterone - pharmacology
Rats
Rats, Inbred Strains
title Anti-inflammatory glucocorticoids inhibit the induction by endotoxin of nitric oxide synthase in the lung, liver and aorta of the rat
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