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.
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Authors | Qi Zhou, Fred A Kummerow |
Journal | Magnesium research
(Magnes Res)
Vol. 25
Issue 1
Pg. 1-11
(Mar 01 2012)
ISSN: 1952-4021 [Electronic] England |
PMID | 22456228
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Arachidonic Acid
- Epoprostenol
- Magnesium
- Calcium
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Topics |
- Arachidonic Acid
(metabolism)
- Biological Transport
(drug effects)
- Calcium
(metabolism)
- Cell Line
- Epoprostenol
(metabolism)
- Humans
- Magnesium
(pharmacology)
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