Magnesium, hypertensive vascular diseases, atherogenesis, subcellular compartmentation of Ca2+ and Mg2+ and vascular contractility.

Abnormal dietary deficiency in Mg as well as abnormalities in Mg metabolism appear to play important roles as risk factors for ischemic heart disease and acute myocardial infarction, namely in hypertensive vascular disease, diabetic vascular disease, insulin resistance, atherosclerosis and vasospasm. Experimental, epidemiological as well as clinical evidence that supports a role for Mg in these risk factors are reviewed. Extracellular Mg ions ([Mg2+]o) exert important actions upon divalent cation metabolism, transport and intracellular release of [Ca2+]i and intracellular free Mg ([Mg2+]i) in both vascular smooth muscle and endothelial cells. Digital imaging microscopy, using molecular fluorescent probes, clearly indicates that both intracellular free Ca2+ and intracellular free Mg2+ are compartmented in both vascular smooth muscle cells and endothelial cells. [Mg2+]o appears to exert important effects on the precise subcellular location and concentration of both [Ca2+]i and [Mg2+]i. Use of specific ion-selective electrodes for [Mg2+]o has revealed that [Mg2+]o can change more rapidly than heretofore believed in cardiovascular pathophysiologic states. The latter new findings therefore suggest that the ionized level of [Mg2+]o is an important determinant of vascular tone, contractility and reactivity.