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

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

Research output: Contribution to journalArticle

81 Citations (Scopus)

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
Externally publishedYes

Fingerprint

Interleukin-1
Endotoxins
Nitric Oxide Synthase
Interleukins
Norepinephrine
Lung
Endotoxemia
Interleukin-1 Receptors
Thoracic Aorta
Tachycardia
Hypotension
Aorta

Keywords

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

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Pharmacology

Cite this

Interleukin-1 contributes to the induction of nitric oxide synthase by endotoxin in vivo. / Szabo, Csaba; Wu, Chin Chen; Gross, Steven S.; Thiemermann, Christoph; Vane, John R.

In: European Journal of Pharmacology, Vol. 250, No. 1, 30.11.1993, p. 157-160.

Research output: Contribution to journalArticle

Szabo, Csaba ; Wu, Chin Chen ; Gross, Steven S. ; Thiemermann, Christoph ; Vane, John R. / Interleukin-1 contributes to the induction of nitric oxide synthase by endotoxin in vivo. In: European Journal of Pharmacology. 1993 ; Vol. 250, No. 1. pp. 157-160.
@article{d6bcae911d5a4eb682c37f27b30f204b,
title = "Interleukin-1 contributes to the induction of nitric oxide synthase by endotoxin in vivo",
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.",
keywords = "Circulatory shock, Cytokine, Endotoxin shock, Vascular hyporeactivity, Vasodilatation",
author = "Csaba Szabo and Wu, {Chin Chen} and Gross, {Steven S.} and Christoph Thiemermann and Vane, {John R.}",
year = "1993",
month = "11",
day = "30",
doi = "10.1016/0014-2999(93)90634-T",
language = "English (US)",
volume = "250",
pages = "157--160",
journal = "European Journal of Pharmacology",
issn = "0014-2999",
publisher = "Elsevier",
number = "1",

}

TY - JOUR

T1 - Interleukin-1 contributes to the induction of nitric oxide synthase by endotoxin in vivo

AU - Szabo, Csaba

AU - Wu, Chin Chen

AU - Gross, Steven S.

AU - Thiemermann, Christoph

AU - Vane, John R.

PY - 1993/11/30

Y1 - 1993/11/30

N2 - 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.

AB - 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.

KW - Circulatory shock

KW - Cytokine

KW - Endotoxin shock

KW - Vascular hyporeactivity

KW - Vasodilatation

UR - http://www.scopus.com/inward/record.url?scp=0027487355&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027487355&partnerID=8YFLogxK

U2 - 10.1016/0014-2999(93)90634-T

DO - 10.1016/0014-2999(93)90634-T

M3 - Article

C2 - 7509750

AN - SCOPUS:0027487355

VL - 250

SP - 157

EP - 160

JO - European Journal of Pharmacology

JF - European Journal of Pharmacology

SN - 0014-2999

IS - 1

ER -