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 journalArticlepeer-review

80 Scopus citations


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
Issue number1
StatePublished - Nov 30 1993
Externally publishedYes


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

ASJC Scopus subject areas

  • Pharmacology


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