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Influence of TNF‐α on vasodilation of isolated rat pulmonary artery rings (1106.17)
Author(s) -
Gassama Abubacarr,
Ray Clare,
Turner Alice,
Egginton Stuart,
Kumar Prem
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1106.17
Subject(s) - myograph , dilator , sodium nitroprusside , vasodilation , vasoconstriction , medicine , electrical impedance myography , vascular smooth muscle , tumor necrosis factor alpha , contraction (grammar) , endocrinology , nitric oxide , smooth muscle
Inflammation promotes endothelial damage leading to vascular smooth muscle cell (VSMC) hyperplasia, vasoconstriction, and vascular remodelling resulting in an increased pulmonary arterial pressure¹. As TNF‐α decreases the bioavailability of NO in systemic vessels, we investigated the effects of TNF‐α on vasodilation in isolated pulmonary arteries (PA). PA segments were isolated from terminally‐anaesthetised Wistar rats and vessel rings were pre‐incubated in DMEM (+/‐ TNF‐α, 1000U/mL) for 2 or 6 hours before mounting on a wire myograph. U46691 (400nM) was used to generate pre‐tone and cumulative dose‐response curves generated for carbachol (CC) and sodium nitroprusside (SNP). Data was normalised to maximal KCl contraction and significance taken as P<0.05. Responses to KCl and U46691 were not significantly different between control and TNF‐α treatments. CC and SNP relaxed pre‐constricted rings but TNF‐α treated rings were significantly less responsive at all doses of either CC or SNP. No difference was noticed between 2 or 6 hours of TNF‐α treatments. This data suggests that TNF‐α pre‐treatment had no effect on the VSMC vasoconstrictor ability but does alter the dilator response to NO.