Interactions of Mg and K on blood vessels--aspects in view of hypertension. Review of present status and new findings.

Considerable experimental as well as clinical evidence has now accumulated to indicate that Mg2+ and K+ deficiencies have probably been overlooked as important causal factors in the etiology of hypertensive disease. Mg2+ ions are important for the regulation of Na+ and K+ transport across cell membranes, including those found in cardiac and vascular smooth muscle cells. Mg2+ activates a Na+-K+-ATPase pump which in turn plays a major role in regulating Na+-K+ transport. Loss of cellular Mg2+ results in the loss of critically important phosphagens: Mg ATP and creatine phosphate. Thus, under conditions where cellular Mg2+ is depleted (e.g. hypoxia, anoxia, ischemia, Mg deficiency, errors in Mg metabolism and/or binding, and transport), the Na+-K+ pump and phosphagen stores will be compromised, leading to alterations in resting membranes (e.g. membrane depolarization). Cellular Mg2+ depletion has been found to result in concomitant depletion of K+ in a number of cells, including cardiac and vascular muscles. Myocardial and vascular injury thus results in an uptake of Na+ and Ca2+, Mg2+ and K+ being lost first. The available evidence indicates that Mg2+ is important in the control of arteriolar tone and blood pressure, primarily via the regulation of vascular membrane Mg2+-Ca2+ exchange sites. A reduction in extracellular Mg2+ (or K+) can produce hypertension, vasospasm and potentiation of vasoconstrictor agents by allowing excess entry of Ca2+, concomitantly the potency of vasodilators is reduced. Alterations in vascular membrane Mg2+ result in 'leaky' arterial and arteriolar membranes thus contributing to the cellular reduction in K+ and the gain of Ca2+ and Na+. These factors seem all-important in the production and etiology of hypertension. Both clinical and experimental forms of hypertension are associated with tissue and plasma deficits of Mg2+. The arterial blood pressure elevation appears to be inversely related to the level of ionized intracellular and plasma Mg2+.