Cytokine-induced venodilatation in humans in vivo: eNOS masquerading as iNOS

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dc.contributor.author Bhagat, K
dc.contributor.author Hingorani, AD
dc.contributor.author Palacios, M
dc.contributor.author Charles, IG
dc.contributor.author Vallance, P
dc.date.accessioned 2011-02-07T06:24:56Z
dc.date.issued 1999-01
dc.identifier.citation Cardiovascular Research, 1999, 41 (3), pp. 754 - 764
dc.identifier.issn 0008-6363
dc.identifier.other C1UNSUBMIT en_US
dc.identifier.uri http://hdl.handle.net/10453/13812
dc.description.abstract Objective: Venodilatation is a feature of endotoxaemia and sepsis. We have tested directly the hypothesis that three cytokines (IL-1?, TNF? and IL-6) generated during endotoxaemia affect venous tone in humans in vivo by increasing NO generation and explored whether the NO comes from the iNOS or eNOS isoform. Design and intervention: Cytokines were given into a superficial vein in very low doses sufficient only to produce changes in the study vessel. The effects of cytokines on the response to noradrenaline were examined. Results: IL-1? increased basal NO-induced dilatation in the study vein, and this was sufficient to attenuate the constrictor response to exogenous noradrenaline or sympathetic stimulation. The effects were maximal at 6 h and both NG-monomethyl-l-arginine and aminoguanidine caused significant reversal of the IL-1? effects. However, no induction of iNOS mRNA was detected in the tissue samples. Instead, mRNA encoding eNOS and GTP cyclohydrolase-1 was detected in all vessels. Conclusion: The simplest explanation of these results is that IL-1? induces expression of GTP cyclohydrolase-1 which leads to increased generation of BH4 and activation of eNOS. This study identifies IL-1? as a key cytokine causing physiologically significant venodilatation in humans by increasing NO generation and suggests that this can occur even in the absence of iNOS expression.
dc.format Yes
dc.publisher Oxford University Press
dc.relation.isbasedon 10.1016/S0008-6363(98)00249-1
dc.title Cytokine-induced venodilatation in humans in vivo: eNOS masquerading as iNOS
dc.type Journal Article
dc.parent Cardiovascular Research
dc.journal.volume 3
dc.journal.volume 41
dc.journal.number 3 en_US
dc.publocation United Kingdom en_US
dc.identifier.startpage 754 en_US
dc.identifier.endpage 764 en_US
dc.cauo.name SCI.Medical and Molecular Biosciences en_US
dc.conference Verified OK en_US
dc.for 1102 Cardiorespiratory Medicine and Haematology
dc.personcode 109028
dc.percentage 100 en_US
dc.classification.name Cardiovascular Medicine and Haematology en_US
dc.classification.type FOR-08 en_US
dc.edition en_US
dc.custom en_US
dc.date.activity en_US
dc.location.activity en_US
dc.description.keywords * Nitric oxide * Veins * Septic shock * GTP cyclohydrolase 1 * Human * Cytokines * Tetrahydrobiopterin * Inducible nitric oxide synthase
pubs.embargo.period Not known
pubs.organisational-group /University of Technology Sydney
pubs.organisational-group /University of Technology Sydney/Faculty of Science
pubs.organisational-group /University of Technology Sydney/Strength - i3
utslib.copyright.status Closed Access
utslib.copyright.date 2015-04-15 12:17:09.805752+10
pubs.consider-herdc false
utslib.collection.history Closed (ID: 3)


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