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- W1605383513 abstract "In a previous study, we found that magnesium deficiency stimulated prostacyclin production and suggested that this stimulation resulted from an enhanced Ca2+ influx induced by magnesium deficiency. In this study, we further examined prostacyclin generation in cultured human umbilical vein endothelial cells after intracellular free calcium content ([Ca2+]i) was altered by addition of diltiazem, nifedipine, verapamil, sodium cyanide (NaCN), ruthenium red or quinidine to a low magnesium medium. The results showed that diltiazem, nifedipine, verapamil and ruthenium red inhibited 45Ca2+ influx, and NaCN and quinidine had no effect on 45Ca2+ influx. However, all of these compounds decreased [Ca2+]i, [3H]arachidonic acid release and prostacyclin production. The reduced [3H]arachidonic acid content in cellular phospholipids caused by low magnesium treatment was not altered by the added compounds. We suggested that arachidonic acid release and prostacyclin production was calcium-dependent in cultured endothelial cells." @default.
- W1605383513 created "2016-06-24" @default.
- W1605383513 creator A5070597794 @default.
- W1605383513 creator A5080618069 @default.
- W1605383513 date "2012-03-01" @default.
- W1605383513 modified "2023-09-27" @default.
- W1605383513 title "Intracellular free calcium content plays a role in low magnesium-induced increases in prostacyclin production" @default.
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- W1605383513 doi "https://doi.org/10.1684/mrh.2012.0306" @default.
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