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Low magnesium stimulated prostacyclin generation in cultured human endothelial cells Volume 21, numéro 3, September 2008

Auteurs
Burnsides Research Laboratory, Department of Veterinary Bioscience, University of Illinois, Urbana, USA, College of Science, Wuhan University of Science and Technology, Wuhan, China, Burnsides Research Laboratory, Department of Agricultural and Biological Engineering, University of Illinois, Urbana, USA

Prostacyclin, synthesized from arachidonic acid, is a strong vasodilator and the most powerful inhibitor known for platelet aggregation. Magnesium deficiency as a risk factor for cardiovascular diseases was related to imbalance of thromboxane and prostacyclin in the vasculature. In this study, we examined the effect of a low level of magnesium on prostacyclin generation in cultured human umbilical vein endothelial cells by measuring arachidonic acid release, 6-keto-prostaglandin F (6-keto-PGF ) production, calcium ( 45Ca 2+) influx, and activity of phospholipase A 2 (PLA 2) and cyclooxygenases (COX), which are the two main enzymes that control the synthesis of prostacyclin. We found that lower levels of magnesium in the culture medium induced a time- and dose-dependent increase in arachidonic acid release. Low magnesium also enhanced 6-keto-PGF production, activated PLA 2 and COX, enhanced 45Ca 2+ influx and decreased the remaining arachidonic acid in phospholipids. Our data indicate that the enhanced 6-keto-PGF production could be due to (1) the stimulated 45Ca 2+ influx resulting in an activation of PLA 2, (2) the increased arachidonic acid liberation from the cell phospholipid, and (3) the activated COX activity. The increased prostacyclin production could provide protection against the cardiovascular effect of thromboxane which was increased by magnesium deficiency.