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Intracellular free calcium content plays a role in low magnesium-induced increases in prostacyclin production.

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.
AuthorsQi Zhou, Fred A Kummerow
JournalMagnesium research (Magnes Res) Vol. 25 Issue 1 Pg. 1-11 (Mar 01 2012) ISSN: 1952-4021 [Electronic] England
PMID22456228 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Arachidonic Acid
  • Epoprostenol
  • Magnesium
  • Calcium
Topics
  • Arachidonic Acid (metabolism)
  • Biological Transport (drug effects)
  • Calcium (metabolism)
  • Cell Line
  • Epoprostenol (metabolism)
  • Humans
  • Magnesium (pharmacology)

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