The Role of Intracellular Magnesium

Magnesium is one of the most abundant ions contrast, in NIDDM patients daily magnesium administration, restoring a more appropriate present in living cells and its plasma concentration is remarkably constant in healthy intracellular magnesium concentration, contributes to improve insulin-mediated glucose subjects. Plasma and intracellular magnesium concentrations are tightly regulated by several uptake. Similarly, in HP patients magnesium administration may be useful in decreasing factors. Among them, insulin seems to be one of the most important. In fact, in vitro and in vivo arterial blood pressure and improving insulinmediated glucose uptake. The benefits deriving studies have demonstrated that insulin may modulate the shift of magnesium from from daily magnesium supplementation in NIDDM and HP patients are further supported by extracellular to intracellular space. Intracellular magnesium concentration has also been shown to epidemiological studies showing that high daily magnesium intake to be predictive of a lower be effective on modulating insulin action (mainly oxidative glucose metabolism), offset calciumincidence of NIDDM and HP. In conclusion, a growing body of studies related excitation-contraction coupling, and decrease smooth cell responsiveness to suggest that intracellular magnesium may play a key role on modulating insulin-mediated glucose depolarizing stimuli, by stimulating Ca 2/ dependent K channels. A poor intracellular uptake and vascular tone. We further suggest that a reduced intracellular magnesium concentration magnesium concentration, as found in non– insulin-dependent diabetes mellitus (NIDDM) might be the missing link helping to explain the epidemiological association between NIDDM and and in hypertensive (HP) patients, may result in a defective tyrosine-kinase activity at the insulin hypertension. q 1997 American Journal of Hypertension, Ltd. Am J Hypertens 1997;10: receptor level and exaggerated intracellular calcium concentration. Both events are responsible 346–355 for the impairment in insulin action and a worsening of insulin resistance in non–insulin