Key result
Incubation of human omental arteries with TNF-alpha attenuated nitric oxide- and prostacyclin-independent endothelial-mediated relaxation, compromising vasorelaxant capacity.
Why the study?
Does TNF-alpha alter endothelial function and vasorelaxation in human omental arteries?
Does TNF-alpha alter endothelial function and vasorelaxation in human omental arteries?
TNF-alpha compromises the vasorelaxant capacity of human systemic arteries in the presence of NO/prostacyclin or EDHF-blockade, highlighting a mechanism for inflammation-induced endothelial dysfunction.
Hypothesis-generating for TNF-alpha in pregnancy endothelial dysfunction; does not yet inform clinical management of hypertension.
OBJECTIVE: To investigate the effect of TNF-alpha on the endothelial function of human systemic arteries. METHODS: Omental arteries were obtained from healthy pregnant women undergoing Cesarean section and examined using isometric wire myography. RESULTS: Incubation with TNF-alpha (1nM) alone did not alter bradykinin-mediated endothelium-dependent relaxation of arteries. However, TNF-alpha did attenuate nitric oxide- (NO) and prostacyclin-independent endothelial-mediated relaxation. Similarly, in vessels constricted with a high potassium solution (60 mM), which inhibits vasodilatation via endothelial-derived hyperpolarising factor (EDHF), TNF-alpha incubation also attenuated bradykinin-induced vasodilatation. CONCLUSIONS: The vasorelaxant capacity of human systemic arteries is compromised by TNF-alpha incubation in the presence of NO/prostacyclin or EDHF-blockade.
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Gillham et al. (2008) studied Healthy pregnancy. TNF-alpha was evaluated on Endothelial-mediated relaxation. Incubation of human omental arteries with TNF-alpha attenuated nitric oxide- and prostacyclin-independent endothelial-mediated relaxation, compromising vasorelaxant capacity.
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