Interleukin-1 contributes to the induction of nitric oxide synthase by endotoxin in vivo

Csaba Szabó, Chin Chen Wu, Steven S. Gross, Christoph Thiemermann, John R. Vane

    Research output: Contribution to journalArticle

    80 Scopus citations

    Abstract

    We investigated the role of interleukin-1 in the induction of a Ca2+-independent nitric oxide (NO) synthase by bacterial endotoxin in vivo. In anaesthetized rats, pretreatment with interleukin-1 receptor antagonist (interleukin-1ra; 16 mg kg-1 i.v., followed by an infusion of 2.4 mg kg-1 h-1) ameliorated the delayed hypotension and tachycardia in response to endotoxin (2 mg kg-1 i.v.). Endotoxaemia for 3 h induced a Ca2+-inependent NO synthase activity in the lung and reduced the contractions to noradrenaline in the thoracic aorta ex vivo. Treatment with interleukin-1ra attenuated both the induction of NO synthase in the lung (by 46±5%) and the endotoxin-induced hyporeactivity to noradrenaline in the aorta. Thus, endogenous interleukin-1 contributes to the induction of NO synthase in response to endotoxin in vivo.

    Original languageEnglish (US)
    Pages (from-to)157-160
    Number of pages4
    JournalEuropean Journal of Pharmacology
    Volume250
    Issue number1
    DOIs
    StatePublished - Nov 30 1993

    Keywords

    • Circulatory shock
    • Cytokine
    • Endotoxin shock
    • Vascular hyporeactivity
    • Vasodilatation

    ASJC Scopus subject areas

    • Pharmacology

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