Endothelial cells in the utero-placental circulation play an important physiological role in maintaining the fetoplacental
vessels in a vasodilated state as these vessels are non-innervated. These endothelial cells produce both prostacyclin
and nitric oxide which in addition to causing vasodilation also prevent platelet aggregation and adhesion of platelets
to endothelial cells. Most investigators are of the opinion that energy metabolism of endothelial cells and ATP generation
is mainly glycolytic. Glycolytic activity in endothelial cells is increased during proliferation to maintain ATP at normal
levels by an increase in the expression of the glucose transporter. More recent studies have reported the existence of a
functional F1F0 ATP synthase on the surface of HUVEC and it has been found to be enzymatically active in the synthesis
of ATP. Additional studies utilizing very early passage HUVEC need to be carried out to ascertain the relative contribution
of oxidative phosphorylation compared with the glycolytic pathway for ATP synthesis in normal pregnancy as well as
in abnormal states like preeclampsia, diabetes, intrauterine injection as well as intrauterine growth restriction.
Keywords: HUVEC, ATP, glycolysis, prostacyclin, nitric oxide.
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