The effect of endotoxin on sympathetic responses in the rat isolated perfused mesenteric bed; Involvement of nitric oxide and cyclo-oxygenase products

Z. Fatehi-Hassanabad, B. L. Furman, J. Parratt

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

1 The effects of endotoxin on the vasoconstrictor responses to sympathetic nerve stimulation (SNS) were investigated in the rat isolated perfused mesenteric bed. 2 Rats received either saline (0.1 ml h-1) or endotoxin (2.5 mg kg-1 h-1) intravenously for 4 h; the mesenteric beds were then isolated, perfused with Krebs and prepared for SNS (50 V, 3 ms, 7-40 Hz). 3 SNS caused a frequency-dependent vasoconstrictor response which was abolished by either tetrodotoxin (10-7 M), prazosin (2.4 x 10-7 M) or guanethidine (2.4 x 10-7 M). 4 In mesenteric vascular beds removed from rats infused with endotoxin, there were markedly impaired vasoconstrictor responses to SNS, although responses to noradrenaline were not modified. 5 Removal of the endothelium with distilled water prevented endotoxin-induced impairment of vasoconstrictor responses to SNS, without modifying these responses in preparations from control rats. 6 Pretreatment with dexamethasone (3 mg kg-1 i.p. 1 h before commencing endotoxin or saline infusions) did not modify responses to SNS in control rats but prevented the effects of endotoxin. 7 Both L-NAME (10-3 M) and indomethacin (10-5 M) restored responses to SNS in preparations from endotoxin-treated rats without modifying these responses in control preparations. However, coadministration of L-NAME and indomethacin markedly augmented responses in both control and endotoxin-treated preparations. 8 The effects of L-NAME were reversed by addition of L-arginine (10-3 M). 9 The data suggest that endotoxin impairs the release of noradrenaline and that this effect is secondary to increased production of nitric oxide and prostanoids, possibly by the endothelium.

Original languageEnglish
Pages (from-to)3316-3322
Number of pages7
JournalBritish Journal of Pharmacology
Volume116
Issue number8
Publication statusPublished - 1995

Fingerprint

Prostaglandin-Endoperoxide Synthases
Endotoxins
Nitric Oxide
Vasoconstrictor Agents
NG-Nitroarginine Methyl Ester
Indomethacin
Endothelium
Norepinephrine
Guanethidine
Prazosin
Tetrodotoxin
Dexamethasone
Prostaglandins
Blood Vessels
Arginine
Water

Keywords

  • Cyclo-oxygenase
  • Dexamethasone
  • Endothelium
  • Endotoxin
  • Mesenteric vascular bed
  • Nitric oxide
  • Sympathetic stimulation

ASJC Scopus subject areas

  • Pharmacology

Cite this

The effect of endotoxin on sympathetic responses in the rat isolated perfused mesenteric bed; Involvement of nitric oxide and cyclo-oxygenase products. / Fatehi-Hassanabad, Z.; Furman, B. L.; Parratt, J.

In: British Journal of Pharmacology, Vol. 116, No. 8, 1995, p. 3316-3322.

Research output: Contribution to journalArticle

@article{49d42dea508c47d98c3987c082e49784,
title = "The effect of endotoxin on sympathetic responses in the rat isolated perfused mesenteric bed; Involvement of nitric oxide and cyclo-oxygenase products",
abstract = "1 The effects of endotoxin on the vasoconstrictor responses to sympathetic nerve stimulation (SNS) were investigated in the rat isolated perfused mesenteric bed. 2 Rats received either saline (0.1 ml h-1) or endotoxin (2.5 mg kg-1 h-1) intravenously for 4 h; the mesenteric beds were then isolated, perfused with Krebs and prepared for SNS (50 V, 3 ms, 7-40 Hz). 3 SNS caused a frequency-dependent vasoconstrictor response which was abolished by either tetrodotoxin (10-7 M), prazosin (2.4 x 10-7 M) or guanethidine (2.4 x 10-7 M). 4 In mesenteric vascular beds removed from rats infused with endotoxin, there were markedly impaired vasoconstrictor responses to SNS, although responses to noradrenaline were not modified. 5 Removal of the endothelium with distilled water prevented endotoxin-induced impairment of vasoconstrictor responses to SNS, without modifying these responses in preparations from control rats. 6 Pretreatment with dexamethasone (3 mg kg-1 i.p. 1 h before commencing endotoxin or saline infusions) did not modify responses to SNS in control rats but prevented the effects of endotoxin. 7 Both L-NAME (10-3 M) and indomethacin (10-5 M) restored responses to SNS in preparations from endotoxin-treated rats without modifying these responses in control preparations. However, coadministration of L-NAME and indomethacin markedly augmented responses in both control and endotoxin-treated preparations. 8 The effects of L-NAME were reversed by addition of L-arginine (10-3 M). 9 The data suggest that endotoxin impairs the release of noradrenaline and that this effect is secondary to increased production of nitric oxide and prostanoids, possibly by the endothelium.",
keywords = "Cyclo-oxygenase, Dexamethasone, Endothelium, Endotoxin, Mesenteric vascular bed, Nitric oxide, Sympathetic stimulation",
author = "Z. Fatehi-Hassanabad and Furman, {B. L.} and J. Parratt",
year = "1995",
language = "English",
volume = "116",
pages = "3316--3322",
journal = "British Journal of Pharmacology",
issn = "0007-1188",
publisher = "Wiley-Blackwell",
number = "8",

}

TY - JOUR

T1 - The effect of endotoxin on sympathetic responses in the rat isolated perfused mesenteric bed; Involvement of nitric oxide and cyclo-oxygenase products

AU - Fatehi-Hassanabad, Z.

AU - Furman, B. L.

AU - Parratt, J.

PY - 1995

Y1 - 1995

N2 - 1 The effects of endotoxin on the vasoconstrictor responses to sympathetic nerve stimulation (SNS) were investigated in the rat isolated perfused mesenteric bed. 2 Rats received either saline (0.1 ml h-1) or endotoxin (2.5 mg kg-1 h-1) intravenously for 4 h; the mesenteric beds were then isolated, perfused with Krebs and prepared for SNS (50 V, 3 ms, 7-40 Hz). 3 SNS caused a frequency-dependent vasoconstrictor response which was abolished by either tetrodotoxin (10-7 M), prazosin (2.4 x 10-7 M) or guanethidine (2.4 x 10-7 M). 4 In mesenteric vascular beds removed from rats infused with endotoxin, there were markedly impaired vasoconstrictor responses to SNS, although responses to noradrenaline were not modified. 5 Removal of the endothelium with distilled water prevented endotoxin-induced impairment of vasoconstrictor responses to SNS, without modifying these responses in preparations from control rats. 6 Pretreatment with dexamethasone (3 mg kg-1 i.p. 1 h before commencing endotoxin or saline infusions) did not modify responses to SNS in control rats but prevented the effects of endotoxin. 7 Both L-NAME (10-3 M) and indomethacin (10-5 M) restored responses to SNS in preparations from endotoxin-treated rats without modifying these responses in control preparations. However, coadministration of L-NAME and indomethacin markedly augmented responses in both control and endotoxin-treated preparations. 8 The effects of L-NAME were reversed by addition of L-arginine (10-3 M). 9 The data suggest that endotoxin impairs the release of noradrenaline and that this effect is secondary to increased production of nitric oxide and prostanoids, possibly by the endothelium.

AB - 1 The effects of endotoxin on the vasoconstrictor responses to sympathetic nerve stimulation (SNS) were investigated in the rat isolated perfused mesenteric bed. 2 Rats received either saline (0.1 ml h-1) or endotoxin (2.5 mg kg-1 h-1) intravenously for 4 h; the mesenteric beds were then isolated, perfused with Krebs and prepared for SNS (50 V, 3 ms, 7-40 Hz). 3 SNS caused a frequency-dependent vasoconstrictor response which was abolished by either tetrodotoxin (10-7 M), prazosin (2.4 x 10-7 M) or guanethidine (2.4 x 10-7 M). 4 In mesenteric vascular beds removed from rats infused with endotoxin, there were markedly impaired vasoconstrictor responses to SNS, although responses to noradrenaline were not modified. 5 Removal of the endothelium with distilled water prevented endotoxin-induced impairment of vasoconstrictor responses to SNS, without modifying these responses in preparations from control rats. 6 Pretreatment with dexamethasone (3 mg kg-1 i.p. 1 h before commencing endotoxin or saline infusions) did not modify responses to SNS in control rats but prevented the effects of endotoxin. 7 Both L-NAME (10-3 M) and indomethacin (10-5 M) restored responses to SNS in preparations from endotoxin-treated rats without modifying these responses in control preparations. However, coadministration of L-NAME and indomethacin markedly augmented responses in both control and endotoxin-treated preparations. 8 The effects of L-NAME were reversed by addition of L-arginine (10-3 M). 9 The data suggest that endotoxin impairs the release of noradrenaline and that this effect is secondary to increased production of nitric oxide and prostanoids, possibly by the endothelium.

KW - Cyclo-oxygenase

KW - Dexamethasone

KW - Endothelium

KW - Endotoxin

KW - Mesenteric vascular bed

KW - Nitric oxide

KW - Sympathetic stimulation

UR - http://www.scopus.com/inward/record.url?scp=0029561921&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029561921&partnerID=8YFLogxK

M3 - Article

VL - 116

SP - 3316

EP - 3322

JO - British Journal of Pharmacology

JF - British Journal of Pharmacology

SN - 0007-1188

IS - 8

ER -