Lysophosphatidylcholine Inhibits Receptor-Mediated Ca 2+ Mobilization in Intact Endothelial Cells of Rabbit Aorta

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Abstract
We have previously reported that lysophosphatidylcholine (LPC), which accumulates in oxidized LDL and atherosclerotic arteries, inhibits endothelium-dependent relaxation and modulates Ca 2+ regulation in cultured bovine aortic endothelial cells. To test the effect of LPC on endothelium-dependent relaxation and endothelial Ca 2+ regulation in intact vessels, we simultaneously measured both isometric tension and endothelial cytosolic free Ca 2+ concentration ([Ca 2+ ] i ), using fura 2, in intact endothelial cells of aortic strips isolated from rabbits. In the aortic strips precontracted with phenylephrine, cumulative addition of acetylcholine (ACh) dose dependently induced endothelium-dependent relaxation, with an increase in endothelial [Ca 2+ ] i , and positive correlation was obtained between these two parameters. LPC (2 to 20 μmol/L) inhibited both ACh (3 μmol/L)-induced endothelium-dependent relaxation and an increase in endothelial [Ca 2+ ] i in a dose-dependent manner. On the other hand, phosphatidylcholine (20 μmol/L) affected neither ACh-induced endothelium-dependent relaxation nor an increase in endothelial [Ca 2+ ] i . LPC had no effect on endothelium-independent relaxation and a decrease in smooth muscle [Ca 2+ ] i induced by nitroglycerin. Thus, the inhibitory effect of LPC on endothelium-dependent relaxation is due to the inhibition of agonist-induced Ca 2+ mobilization in vascular endothelial cells, which is an essential step in the synthesis of endothelium-derived relaxing factor.

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