Mechanisms responsible for vasodilation upon magnesium infusion in vivo: clinical evidence

A number of studies have shown that intravenous administration of magnesium (Mg) is an effective treatment for acute coronary syndromes. While mechanisms such as antiarrhythmic, antithrombotic, and myocardial cytoprotective effects may be involved, a vasodilatory effect is among the likely beneficial effects of Mg infusion. The vasodilatory effect of Mg is incompletely understood. On one hand, Mg can act as a physiologic calcium-antagonist, but in addition interest recently has been focused on whether endothelium-derived nitric oxide is involved in Mg-induced vasodilation. Another issue in Mg-induced vasodilation is whether the specific Mg salt administered influence the degree of vasodilation. Although Mg sulphate has undergone more clinical studies than Mg chloride, experimental studies suggest that Mg chloride influences vasculature more than Mg sulphate. No clinical research has investigated whether the vasodilatory effect of Mg differs according to the associated anion administered. The present review includes evidence concerning mechanisms of the vasodilatory effect of Mg including endothelium-derived nitric oxide, as well as the possible differences between different Mg salts.