Decreased Cell Membrane Magnesium in Some Essential Hypertension Patients

Abstract

The concentrations of total ([T-Mg]), ultrafilterable ([UF-Mg]), and protein-bound or nonfilterable ([NF-Mg]) magnesium were measured in the plasma and in the intracellular compartment of blood from 8 essential hypertensive patients and 9 normotensive subjects. In the former, [T-Mg] was unchanged in the plasma but decreased in whole blood due to decreases of both [UF-Mg] and [NF-MG]; [UF-Mg] was increased in plasma but decreased intracellularly while [NF-Mg] was decreased in plasma and unchanged intracellularly. These concentrations correlated significantly with the average blood pressures. Decreased Mg binding to the erythrocyte membrane was also observed in 13 additional essential hypertensive patients. This decreased binding may well be responsible for the decreased intracellular [UF-Mg] in the blood of such patients. The cause of the decreased Mg binding to the erythrocyte membrane is unknown, but the binding is returned to normal by incubating erythrocytes from essential hypertensive patients with blood plasma from normotensive subjects. Decreased Mg binding to cell membranes must also occur in frankly Mg-deficient patients, some of whom, as a consequence of the primary deficiency of this mineral, are hypertensive. Normal Mg binding to erythrocyte membranes was observed in two patients with hypertension indicating that hypertension per se does not cause decreased Mg binding to cell membranes. These observations suggest that decreased Mg binding to cell membranes may be an important contributing factor in some cases of essential hypertension.

Evidence that the etiology of the syndrome containing type 2 diabetes mellitus results from abnormal magnesium metabolism

“…This fact, that these 2 ions are bound together and that their actual concentrations can change, but only concomitantly, is represented by the expression ''the intracellular [Mg 2+ ] and its dependent [MgATP 2-].'' This concept is consistent with the analytical results obtained with the erythrocytes of essential hypertensive subjects (Mattingly et al 1991;Resnick et al 1984;Matuura et al 1987) and presumably occurs in all their somatic cells.…”

“…Nevertheless, the process by which this ion enters somatic cells, that is, cells other than endothelial cells, has been considered to be exclusively by diffusion. In contrast to this simple concept, however, our studies (Mattingly et al 1991;Wells et al 2004;Wells and Agrawal 1992) of this cell-entering process have revealed that it is genetically and otherwise controlled.…”

“…This occurs normally in the cells of persons who are not at risk for type 2 diabetes mellitus and its associated diseases, such as Na + -sensitive hypertension and hyperinsulinemia. The intracellular concentration of bound (i.e., non-filterable) magnesium ions remains constant even when the MgBD is present (Mattingly et al 1991), but may not in dietary magnesium deficiency.…”

“…In studies of randomly selected, non-obese patients who had essential hypertension (Mattingly et al 1991) and overt type 2 diabetes mellitus (Wells et al 2004), all were found to have a magnesium-binding defect (MgBD) (Wells and Agrawal 1992). This defect is expressed as a decreased content of tightly bound magnesium ions in the plasma membranes of somatic cells (Mattingly et al 1991) and is inherited (Wells et al 2004).…”

“…This defect is expressed as a decreased content of tightly bound magnesium ions in the plasma membranes of somatic cells (Mattingly et al 1991) and is inherited (Wells et al 2004). It reduces the normal, maximum allowable concentration of intracellular Mg 2+ ions and also that of the complex of magnesium and ATP (MgATP 2-), which is the currency of metabolic energy in the cell (Leghninger 1975).…”