Intracellular free calcium content plays a role in low magnesium-induced increases in prostacyclin production
作者： Qi Zhou , Fred A Kummerow
关键词: Prostacyclin 、 Endocrinology 、 Magnesium deficiency (medicine) 、 Calcium 、 Chemistry 、 Ruthenium red 、 Verapamil 、 Magnesium 、 Arachidonic acid 、 Sodium cyanide 、 Internal medicine 、 Clinical biochemistry 、 Biochemistry 、 Molecular biology
摘要: In a previous study, we found that magnesium deficiency stimulated prostacyclin production and suggested this stimulation resulted from an enhanced Ca2+ influx induced by deficiency. further examined generation in cultured human umbilical vein endothelial cells after intracellular free calcium content ([Ca2+]i) was altered addition of diltiazem, nifedipine, verapamil, sodium cyanide (NaCN), ruthenium red or quinidine to low medium. The results showed verapamil inhibited 45Ca2+ influx, NaCN had no effect on influx. However, all these compounds decreased [Ca2+]i, [3H]arachidonic acid release production. reduced cellular phospholipids caused treatment not the added compounds. We arachidonic calcium-dependent cells.
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