Magnesium Research


Effects of magnesium on prostacyclin synthesis and intracellular free calcium concentration in vascular cells Volume 17, numéro 1, March 2004

First Department of Internal Medicine, Fukui University, 23 Shimoaizuki, Matsuoka‐cho, Fukui 910‐1193, Japan

This study investigated the effects of extracellular magnesium concentration ([Mg 2+ ]e; 0.3‐3 mM) on intracellular free calcium concentration ([Ca 2+ ]i) and prostacyclin (PGI 2) production in cultured human umbilical vein endothelial cells (HUVEC) and vascular smooth muscle cells from rats (VSMC) under basal and agonist‐stimulated conditions. We used histamine as agonist which increases [Ca 2+ ]i and PGI 2 production in HUVEC, norepinephrine in VSMC. [Mg 2+ ]e dose‐dependently increased basal and agonist‐stimulated PGI 2 production in both cells. [Mg 2+ ]e dose‐dependently reduced basal [Ca 2+ ]i in VSMC, but did not influence in HUVEC. In both cells, increasing [Mg 2+ ]e reduced agonist‐stimulated [Ca 2+ ]i responses. Furthermore, [Mg 2+ ]e dose‐dependently reduced agonist‐stimulated [Ca 2+ ]i in Ca 2+ ‐free buffer, indicating intracellular Ca 2+ release. In VSMC, 10 ‐‐6 M diltiazem and 10 ‐7 M nifedipine, Ca 2+ channel blockers, reduced agonist‐stimulated [Ca 2+ ]i as well as 3 mM Mg 2+, but did not affect PGI 2 production. [Mg 2+ ]e amplified dose‐dependently arachidonic acid‐induced PGI 2 production in both cells, suggesting the activation of cyclooxygenase and\or PGI 2 synthetase. Our results suggest that [Mg 2+ ]e influences intracellular Ca 2+ mobilization of not only vascular smooth muscle cells but also endothelial cells by inhibiting both Ca 2+ influx and intracellular Ca 2+ release. [Mg 2+ ]e enhances PGI 2 production in both types of cells, although the mechanism is likely to be independent from Ca 2+ mobilization.