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• W2022382603 abstract "Vascular serotonin 5-HT1 receptors have quiescent constrictor activity that is activated by other vasoactive agents such as histamine. Previously, we observed that the 5-HT1-selective agonist 5-carboxamidotryptamine (5-CT) potentiated histamine-stimulated arachidonic acid (AA) mobilization and prostaglandin production in human aortic endothelial cells (HAEC). In the present study, 5-CT was found to potentiate histamine-stimulated calcium mobilization but had no effect on intracellular calcium when added alone. Treatment of HAEC with human low-density lipoprotein (LDL) for 20 hours inhibited the histamine- plus 5-CT-stimulated production of prostaglandin F2α (PGF2α) and the prostacyclin metabolite 6-keto-PGF1α. However, the effects of histamine and histamine potentiation by 5-CT on intracellular Ca2+ mobilization and AA release were resistant to LDL treatment. Conversely, the subsequent receptor-independent conversion of AA to prostaglandins was inhibited by LDL. These results demonstrate that histamine and serotonin receptor activity, measured as the stimulation of Ca2+ and AA mobilization, is resistant to LDL exposure under mild oxidizing conditions, whereas the receptor-independent synthesis of prostaglandins is inhibited by LDL. The results also suggest that the LDL-stimulated mobilization of cellular AA is responsible for the LDL-mediated inhibition of prostaglandin synthesis. These findings suggest a mechanism by which LDL and/or atherosclerosis could promote the vascular liberation of AA that is not converted to endothelium-derived prostaglandins and is therefore available as substrate for the production of other eicosanoids." @default.
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• W2022382603 date "2004-11-01" @default.
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• W2022382603 title "Low-Density Lipoprotein Inhibits Receptor-Mediated Prostaglandin Synthesis without Affecting Calcium and Arachidonic Acid Mobilization in Human Endothelial Cells" @default.
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• W2022382603 doi "https://doi.org/10.1097/00005344-200411000-00015" @default.
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