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Until recently the physiological role of magnesium was essentially ignored. However, with the development of new technologies to measure the intracellular free concentration of magnesium ([Mg2+]i), the biologically important fraction, there has been an explosion of interest in the molecular, biochemical, physiological and pharmacological functions of magnesium. In addition improved methods for assessing magnesium status in the clinic have contributed to the further understanding of magnesium regulation in health and disease. Magnesium deficiency is now considered to contribute to many diseases and the role for magnesium as a therapeutic agent is being tested in numerous large clinical trials. This review focuses on clinical manifestations associated with magnesium deficiency and highlights the clinical significance of hypermagnesemia. Specific clinical conditions in which magnesium deficiency has been implicated to play a pathophysiological role, namely hypertension, ischemic heart disease, arrhythmias, prec-eclampsia, asthma and critical illness will be discussed and the possible therapeutic role of magnesium will be considered. Although there is still much to be learnt regarding the exact role of magnesium in clinical medicine, there are two conditions where magnesium is now considered the therapeutic agent of choice, pre-eclampsia and torsades de pointes. Future research, both at the fundamental and clinical levels, will certainly facilitate our understanding of how magnesium contributes to pathological processes and under what circumstances it should be used therapeutically.
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PMID:Magnesium in clinical medicine. 1497 44

Preeclampsia is a pregnancy disorder of unknown origin, characterized by vasospasm, elevated blood pressure, and increased neuromuscular irritability, features common to syndromes of magnesium deficiency. Evidence of serum and ionized magnesium metabolism disturbances have been observed in women with preeclampsia. This and the therapeutic utility of magnesium in preeclampsia led us to investigate the extent to which an endogenous tissue magnesium deficiency might be present in and contribute to its pathophysiology. We used (31)P nuclear magnetic resonance spectroscopy to noninvasively measure in situ intracellular-free magnesium levels in brain and skeletal muscle of fasting nonpregnant women (n=12), and of third trimester women with uncomplicated pregnancies (n=11) and preeclampsia (n=7). Compared with nonpregnant controls (brain 519+/-59 micromol/L; muscle 604+/-34 micromol/L), brain and skeletal muscle intracellular magnesium levels were significantly lower in both normal pregnant (brain 342+/-23 micromol/L; muscle 482+/-40 micromol/L; P=0.05 for both tissues) and preeclamptic women (brain 229+/-17 micromol/L; muscle 433+/-46 micromol/L; P=0.05 for both tissues). Brain intracellular magnesium was further reduced in preeclamptics compared with normal pregnant subjects (P=0.05). For all pregnant subjects, blood pressure was significantly and inversely related to the concomitantly measured intracellular magnesium level in brain (systolic, r=-0.59, P=0.01; diastolic, r=-0.52, P=0.02) but not in muscle. Cellular magnesium depletion is characteristic of normal pregnancy and may be one factor contributing to the pathophysiology of preeclampsia. Furthermore, the influence of central nervous system factors on blood pressure may be mediated, at least in part, by ambient intracellular magnesium levels.
Hypertension 2004 Sep
PMID:Cellular-free magnesium depletion in brain and muscle of normal and preeclamptic pregnancy: a nuclear magnetic resonance spectroscopic study. 1526 10

Vascular disease is one of the complicating features of diabetes mellitus. Magnesium deficiency has recently been proposed as a novel factor implicated in the pathogenesis of diabetes complications. Several studies have indicated that hypertension in diabetic patients is an independent altered reaction of blood vessels to neurotransmitters and circulating hormones. Since magnesium has been proposed to decrease vascular sensitivity to vasoconstrictor agents, the present study was designed to determine whether chronic magnesium sulfate administration could prevent vascular complications of STZ-induced diabetes in rats. The animals were divided into six groups: two groups served as controls and received tap water for 8 weeks, while in the other four groups, made diabetic with a single IV injection of 40 mg/kg STZ, two groups treated with magnesium sulfate (10 g/L) added to the drinking water, and the other two groups received tap water only. After 8 weeks, in 3 groups (control, diabetic and Mg-treated), left common carotid artery was cannulated for continuous recording of blood pressure. All animals in these groups were decapitated and blood samples were drawn for glucose, Ca and Mg measurements. In the 3 remaining groups (again divided into control, diabetic and Mg-treated), the mesenteric vascular bed was perfused according to the McGregor method, and descending thoracic aortas were used for measurement of elasticity. In diabetic rats, plasma glucose was significantly increased and plasma magnesium was significantly decreased compared to controls and Mg-treated animals. Although plasma magnesium of Mg-treated animals increased significantly, it failed to reach to the magnesium level of the control group. Ca/Mg ratio was also increased compared to the control and Mg-treated animals. Mean arterial blood pressure in diabetics was significantly higher than control and Mg-treated rats. Similarly, there was a significant difference in mean arterial blood pressure of Mg-treated rats compared to control animals. Baseline perfusion pressure of diabetic group was significantly higher than control and Mg-treated groups with intact and denuded endothelium. Magnesium sulfate treatment decreased mean perfusion pressure of mesenteric vascular bed in intact and denuded endothelium in comparison with non-treated diabetic rats. There was a significant increase in passive tension in the aorta of diabetic rats compared to control and Mg-treated rats. However, there was no significant difference between Mg-treated and control rats. From the results of this study it may be concluded that magnesium could control STZ-induced diabetes and prevent its vascular complications.
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PMID:Oral magnesium administration prevents vascular complications in STZ-diabetic rats. 1568 Mar 10

As the understanding for the mechanism of absorption and metabolism has not been clarified adequately, a lot of works about these issues are still carrying on. Changes in maternal blood and intracellular magnesium concentration during the early stage of pregnancy suggest magnesium may play important roles around the period of implantation. Alternation in absorption of the mineral from colon, in levels of maternal blood and those of intracellular magnesium, or in urinary excretion of magnesium during pregnancy suggest that contents of magnesium in the whole maternal body tend to be decreased with the course of pregnancy. On the other hand, in preeclamptic women lack of magnesium is existed showing a pathological level compared to normal pregnant women. The magnesium deficiency is speculated to have a relation with vascular hypertonus or eclamptic seizures. Magnesium sulfate is frequently used for first choice drug, as it is effective to improve the hypertension of preeclampsia, to prevent or to cure the seizures of eclampsia. The administration of magnesium sulfate to preeclamtic women is reasonable to improve magnesium deficiency, which may be one of pathophysiological aspects of preeclampsia.
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PMID:[Toxemie of pregnancy and magnesium]. 1569 59

Magnesium status has a direct effect upon the relaxation capability of vascular smooth muscle cells and the regulation of the cellular placement of other cations important to blood pressure - cellular sodium:potassium (Na:K) ratio and intracellular calcium (iCa(2+)). As a result, nutritional magnesium has both direct and indirect impacts on the regulation of blood pressure and therefore on the occurrence of hypertension. Hypertension occurs when cellular Na:K ratios become too high, a consequence of a high sodium, low potassium diet or, indirectly, through a magnesium deficient state which causes a pseudo potassium deficit. Like wise, magnesium deficiency alters calcium metabolism, creating high iCa(2+), low serum calcium and low urinary calcium states even when calcium intake is adequate. High iCa(2 + ) and high cellular Na:K ratio both occur when cellular magnesium becomes too low and the Mg-ATP driven sodium-potassium pump and calcium pump become functionally impaired. High iCa(2+) has several vasoconstrictive effects which lead to hypertension, an indirect result of low magnesium status. Dietary calcium is directly proportional to dietary magnesium. Serum magnesium does not reflect true magnesium status as do intracellular magnesium measurements. Several studies on the effect of calcium on blood pressure need these added considerations of magnesium status to fully understand the impact of the Mg:Ca ratio as the primary cause of hypertension and other aspects of Syndrome X. Magnesium supplementation above 15 mmol per day are required to normalize high blood pressure in unmedicated hypertensive patients while 15 mmol per day will lower high blood pressure in patients treated with anti-hypertensive medications. In most humans, healthy blood pressure depends upon a balance of both Na:K and Mg:Ca ratios at both cellular and whole body levels which, in turn, require adequate, long-term intakes of nutritional magnesium. The knowledge that low magnesium causes imbalance in both cellular and physiological calcium widens our view of the studies showing hypertensives have abnormal calcium metabolism.
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PMID:[Magnesium and hypertension]. 1569 66

Electrolyte balance is a critical issue in managing comorbid conditions in both diseased and elderly patients. Patients with hypertension and diabetes need careful regulation of their calcium and magnesium levels, whereas in patients with congestive heart failure, sodium and potassium levels also are critical. Herein we report the outcome of a round table discussion at which issues of renal magnesium clearance, magnesium and arrhythmic risk, ion balance in heart failure, diabetes, ischemic stress, oxidative stress in the cardiomyopathy of magnesium deficiency, roles of magnesium and potassium in bone metabolism and the aging population, and the role of electrolyte balance in hypertension have been discussed. In all these issues the maintaining homeostasis of potassium and magnesium is critical and the various therapies that impact on retaining these ions were discussed. Hallmark studies, i.e., Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial and Studies of Left Ventricular Dysfunction, have provided insight into treatment of patients with cardiovascular and progressive heart failure. These studies and the availability of potassium- and magnesium-sparing diuretics for use in these disorders provide relevant perspectives for treatment.
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PMID:Potassium, magnesium, and electrolyte imbalance and complications in disease management. 1577 33

Numerous studies have suggested that magnesium ion (Mg(2+)) plays an important role in pathogenesis of cardiovascular diseases including hypertension, ischemic heart disease. Hypomagnesemia is often associated with the imbalance of sodium, potassium, and calcium ions. Magnesium deficiency can occur frequently in alcoholics, and in patients with hypertension, congestive heart failure, myocardial infarction. Magnesium deficiency induces an increase in intracellular Ca(2+) concentration in cardiac myocytes, formation of reactive oxygen species, production of inflammatory cytokines, leading to the development of ischemic heart disease, congestive heart disease, sudden cardiac death, atherosclerosis, and arrhythmia. In addition, catecholamines can evoke marked Mg(2+)efflux which is associated with a concomitant increase in the force of contraction of the heart. While many of the mechanisms remains elusive, the beneficial effects of magnesium on the myocardium appear to be convincing. Further studies will be necessary to elucidate the molecular basis of the cardio-protective effects of magnesium.
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PMID:[Role of magnesium in cardiac metabolism]. 1627 16

The purpose of this review is to summarize experimental findings showing that magnesium modulates cellular events involved in inflammation. Experimental magnesium deficiency in the rat induces after a few days a clinical inflammatory syndrome characterized by leukocyte and macrophage activation, release of inflammatory cytokines and acute phase proteins, excessive production of free radicals. Increase in extracellular magnesium concentration, decreases inflammatory response while reduction in the extracellular magnesium results in cell activation. Because magnesium acts as a natural calcium antagonist, the molecular basis for inflammatory response is probably the result of modulation of intracellular calcium concentration. The priming of phagocytic cells, the opening calcium channel and activation of N-methyl-d-aspartate (NMDA) receptors, the activation of nuclear factor-kappa B (NFkappaB) have been considered as potential mechanisms. Moreover, magnesium deficiency induces a systemic stress response by activation of neuro endocrinological pathways. As nervous and immune systems interact bidirectionally, the roles of neuromediators have also been considered. Magnesium deficiency contributes to an exaggerated response to immune stress and oxidative stress is the consequence of the inflammatory response. Inflammation contributes to the pro-atherogenic changes in lipoprotein metabolism, endothelial dysfunction, thrombosis, hypertension and explains the aggravating effect of magnesium deficiency on the development of metabolic syndrome. Further studies are still needed to assess more accurately the role of magnesium in immune response in humans, but these experimental findings in animal models suggest that inflammation is the missing link to explain the role of magnesium in many pathological conditions.
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PMID:Magnesium and the inflammatory response: potential physiopathological implications. 1671 75

Magnesium affects blood pressure by modulating vascular tone and reactivity. It acts as a calcium channel antagonist, it stimulates production of vasodilator prostacyclins and nitric oxide and it alters vascular responses to vasoactive agonists. Magnesium deficiency has been implicated in the pathogenesis of hypertension with epidemiological and experimental studies demonstrating an inverse correlation between blood pressure and serum magnesium levels. Magnesium also influences glucose and insulin homeostasis, and hypomagnesemia is associated with metabolic syndrome. Although most epidemiological and experimental studies support a role for low magnesium in the pathophysiology of hypertension, data from clinical studies have been less convincing. Furthermore, the therapeutic value of magnesium in the management of hypertension is unclear. The present review addresses the role of magnesium in the regulation of vascular function and blood pressure and discusses the implications of magnesium deficiency in experimental and clinical hypertension, in metabolic syndrome and in pre-eclampsia.
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PMID:Role of magnesium in hypertension. 1676 12

A case control study was carried out to detect the relation between magnesium deficiency and diabetic retinopathy and to study other risk factors for diabetic retinopathy. The study involved 30 cases with diabetic retinopathy, 30 diabetics and 30 non-diabetics with normal retina as controls. Serum magnesium was significantly lower in the diabetic control group than both other groups. Significant association between diabetic retinopathy and hypertension, poor control of blood sugar, irregularity in drug treatment, lack of routine fundus examination, high gravidity and low socioeconomic status were found. Multiple regression analysis was used to adjust for all variables mentioned. Magnesium deficiency was found to be statistically significantly associated with diabetic retinopathy after considering the effects of other variables.
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PMID:Magnesium deficiency and other risk factors for diabetic retinopathy. 1721 26


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