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
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
2+ influx, and NaCN and quinidine had no effect on
2+ influx. However, all of these compounds decreased [Ca
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.