John Libbey Eurotext

Magnesium Research

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Intracellular free calcium content plays a role in low magnesium-induced increases in prostacyclin production Volume 25, numéro 1, March 2012

Auteurs
Burnsides Research Laboratory, Department of Comparative Biosciences, University of Illinois, 1208 W. Pennsylvania Avenue, Urbana, IL 61801, USA

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.