In vascular smooth muscle cells magnesium acts intracellularly and extracellularly as a calcium antagonist to inhibit contractility. In animal models it blocks calcium entry into these cells via voltage-and receptor-mediated channels. Inhibition of calcium entry into cells decreases the contractile actions of vasoactive agents. Intracellulary, calcium antagonism is related to the decreased influx and increased efflux of calcium leading to decreased intracellular free calcium and decreased contractility via decreased cGMP. It has also been shown to stimulate prostacyclin and nitric oxide release from vascular endothelium causing vasodilation.
Magnesium also indirectly affects vascular contractility by inhibiting the release of catecholamines both from the adrenal medulla and peripheral adrenergic terminals resulting in decreased vasoconstriction.
In obstetrics, Mg decreases uterine tone through relaxation of uterine blood vessels and uterine smooth muscle.
References
- W J Fawcett, E J Haxby, D A Male Magnesium: physiology and pharmacology.Br J Anaesth: 1999, 83(2);302-20 Link
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