Magnesium Research
MENUIntracellular free calcium content plays a role in low magnesium-induced increases in prostacyclin production Volume 25, numéro 1, March 2012
Illustrations
- Mots-clés : arachidonic acid release, prostacyclin production, [Ca 2+] i, low magnesium, cultured endothelial cells
- DOI : 10.1684/mrh.2012.0306
- Page(s) : 1-11
- Année de parution : 2012
In a previous study, we found that magnesium deficiency stimulated prostacyclin production and suggested that this stimulation resulted from an enhanced Ca 2+ 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 ([Ca 2+] 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 45Ca 2+ influx, and NaCN and quinidine had no effect on 45Ca 2+ influx. However, all of these compounds decreased [Ca 2+] 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.