Influence of TNF‐α on vasodilation of isolated rat pulmonary artery rings (1106.17)

Abstract

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.