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Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

Elderly patients have a higher incidence of symptomatic cardiac arrhythmias and greater management problems than younger patients. This is due to the frequency of occult and overt cardiovascular disease, reduction in cardiac reserve as a consequence of the aging process, and coexistence of other disorders which provide a substrate for iatrogenic disease. The last problem is largely due to electrolyte disturbances induced by diuretic therapy for hypertension and heart failure. The major electrolyte disturbance implicated in arrhythmogenesis is diuretic-induced hypokalemia. There is no doubt that arrhythmias are caused by severe hypokalemia (less than 2.5 mEq/l), or by a milder degree of hypokalemia in digitalis-treated patients or those with left ventricular hypertrophy, but the literature contains conflicting data regarding the importance of milder hypokalemia. The most compelling study in support of its importance used a crossover study design in hypertensive patients with coronary disease and showed that mild degrees of hypokalemia induced by thiazide diuretics increased the tendency to arrhythmia when compared with normokalemia on a potassium-sparing diuretic. Diuretic-induced magnesium deficiency is also regarded by some to be as important as hypokalemia, but the evidence is less extensive. Thus, it appears reasonable to avoid hypokalemia and hypomagnesemia. The optimum therapeutic approach in using diuretics is to keep the dose as low as possible, restrict dietary sodium, and add potassium supplements. Since, in many cases of hypertension, hypokalemia is due to secondary hyperaldosteronism, the use of angiotensin-converting enzyme inhibitors is another therapeutic approach that is effective in hypertension and heart failure.
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PMID:Arrhythmias, electrolytes, and ACE inhibitor therapy in the elderly. 344 May 24

Investigation of coronary heart disease manifesting as sudden death has highlighted the role of electrolyte disturbances in arrhythmogenesis. The identification of the 3 major cardiac risk factors--hyperlipidaemia, hypertension and smoking--does not fully explain sudden death in asymptomatic patients with an abnormal ECG. Sudden death is usually ascribed to cardiac arrhythmia whose pathogenesis has 3 possible mechanisms affecting the electrical properties of the heart. Thiazide diuretics are known to deplete potassium and magnesium in the body and while magnesium deficiency has been especially associated with cardiac rhythmicity, potassium levels modulate the cellular effects of calcium in the myocardium. In patients with ischaemic heart disease, both hypokalaemia and hypomagnesaemia correlate with the frequency of serious arrhythmias and even in ambulatory hypertensive patients on diuretics, it is important to preserve electrolyte homeostasis. There is, however evidence to suggest that some patients are more susceptible to diuretic-induced arrhythmias and in these patients even mild hypokalaemia can cause ventricular arrhythmias, and age may be a contributory factor. The risk of thiazide-induced arrhythmias has yet to be confirmed.
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PMID:Electrolyte abnormalities and ventricular arrhythmias. 352 91

The influence of long-term alterations in dietary magnesium intake on blood pressure and on the antihypertensive effect of the calcium antagonist nifedipine was investigated in normotensive Wistar-Kyoto (WKY) and in spontaneously hypertensive rats (SHR). The rats were fed a diet either high (1%), normal (0.1%), or low (0.01%) in magnesium for 12 weeks (WKY) and 20 weeks (SHR), respectively. Nifedipine was added to the diet for 4 weeks in concentrations of 300 and 1000 ppm. Each dose was given for 2 weeks. Plasma and intraerythrocytic concentrations of sodium, potassium, and magnesium were measured before and at the end of nifedipine treatment. Blood was obtained by cardiac puncture. In the WKY and SHR, blood pressure was not influenced by magnesium intake. The blood pressure-lowering effect of nifedipine was most pronounced on normal dietary magnesium and was significantly suppressed in the magnesium-deficient rats. Plasma and intracellular total magnesium concentrations were consistently increased during high and reduced during low dietary intake of the ion. Intracellular sodium concentration increased during magnesium deficiency and was normalized by nifedipine. The marked and long-term alterations in plasma and intracellular concentrations of magnesium did not influence arterial blood pressure levels in either the normotensive WKY or the SHR. Therefore, dietary magnesium intake does not appear to play an important role in long-term regulation of blood pressure in rats. However, magnesium depletion attenuates the blood pressure-lowering effect of nifedipine.
Hypertension 1987 Feb
PMID:Influence of magnesium on blood pressure and the effect of nifedipine in rats. 381 11

From the pre-natal follow-up it was remarkable that cases have been admitted relatively late. Hints to a possible development of preeclampsia could be seen from patients history or the routine check up, for example the registration of edema, fetal growth retardation and oligohydramnios. For early diagnosis of preeclampsia we recommend: Calculation of mean arterial blood pressure or its non-invasive measurement; determination of hematocrit, uric acid and total plasma protein (in particular hemorheologic measurements). Hypomagnesemia in preeclampsia, as described by some authors, was also seen in our cases. The complex symptomatology of preeclampsia could be attributed to a generalised disturbance of microcirculation, which leads to definite reactions of the organs concerned. The microcirculatory failure is caused by vasoconstriction, hemoconcentration, hyperviscosity and hypercoagulation (up to DIC and consumption coagulopathy). The resulting symptoms and syndromes can be: EPH, HELLP, hemolytic-uremic Syndrome, hepato-renal Syndrome, thrombocyte and antithrombin III deficiency etc. The drug of choice for treatment of preeclampsia is magnesium sulfate. Its application is based on long-term clinical experience and new aspects on the physiologic and pharmacologic role of magnesium. The recommendations of the German High Blood Pressure League to use calcium antagonists as a basis in the treatment of high blood pressure can be fulfilled particularly in pregnancy by the physiologic calcium antagonist Mg++. Magnesium sulfate should be given in a dosage of 24-72 g daily. The dose should also be made dependent from urinary output. Further treatment patterns of preeclampsia should be adjusted according to each case. The present results also support our hypothesis that magnesium deficiency (besides predisposing factors) could be responsible for the development of preeclampsia (present model shown in detail). Consequently, the early and long-term substitution of magnesium in pregnancy could help reduce preeclampsia.
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PMID:[Pathophysiology and clinical aspects of pre-eclampsia]. 404 84

Particular investigations and hints from the literature led to suggest that Magnesium deficiency in pregnancy plays a role in the development of pregnancy-induced hypertension as well as gestosis or pre-eclampsia. The integration of the already known facts about the physiopathology of Magnesium deficiency to those of the pathogenesis of gestosis led to the concept of a gestosis model which is based on Magnesium deficiency. In this way Magnesium deficiency represents the cause of (essential) gestosis. Further investigations should be done in this direction.
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PMID:[Current concepts in the pathogenesis of gestosis with special reference to magnesium deficiency]. 637 81

In studies concerning risk factors for cardiovascular diseases, a number of reports have emphasized the influence of lipids, but the role of dietary minerals other than sodium has been less studied. However, epidemiological studies have suggested that dietary intake of magnesium and potassium may be involved in such pathogenesis. Studies of the influence of magnesium deficiency on arteriosclerosis include its effect on the initial lesion, altered metabolism of elastin, proliferation of collagen, calcification, lipid metabolism, platelet aggregation and hypertension. Magnesium and potassium metabolism are closely related and magnesium is required for maintaining the level of cellular potassium. As a consequence, magnesium and potassium deficiency frequently occur together and potassium deficiency may be an aggravating factor in pathogenesis. The development of the initial lesion in the arterial wall may be facilitated by loss of cellular magnesium and potassium. Experimental magnesium deficiency induces arterial damage, a loss of magnesium and potassium and an increase in the calcium and sodium content of the cell. Experimental models that have been used to produce cardiovascular lesions induce similar changes and losses of major intracellular cations may affect the main metabolic processes of the cell. This report summarizes the experimental evidence that magnesium deficiency may affect several different stages involved in arteriosclerosis and that potassium deficiency may exacerbate this. Magnesium deficiency results in vascular calcification. Experiments indicate that elastin is the site of the initial calcification and the metabolism of elastin is altered. This vascular lesion then brings about an increase in the collagen content of the wall. Low magnesium status could probably affect this process by slowing collagen resorption and lead to an irreversible accumulation of connective tissue. Results showing a different distribution of the various types of lipoprotein during experimental magnesium deficiency strongly suggest that lipid exchange between the vessel walls and blood can be modified. Severe magnesium deficiency in weanling rats produces a marked hypertriglyceridemia, a decrease in the percentage of cholesterol transported by HDL lipoprotein and a reduction in LCAT activity. The decreased clearance of circulatory triglycerides appears to be the major mechanism contributing to hyperlipemia. Magnesium deficiency could therefore contribute to accumulation of vascular lipid. Magnesium and potassium depletion have also been reported in diabetes and the vascular implications of this should be considered.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of magnesium and potassium in the pathogenesis of arteriosclerosis. 639 44

Diuretic agents influence the renal handling of magnesium, causing increased losses of the ion. Continuing magnesium losses may, in the long term, result in a magnesium deficiency. 296 patients with congestive heart failure or arterial hypertension receiving long term diuretic therapy were studied by skeletal muscle biopsies to assess their magnesium status. 65% of the congestive heart failure patients and 42% of the patients with arterial hypertension were found to have subnormal values for skeletal muscle magnesium. Studies with the potassium-sparing diuretics amiloride, spironolactone and triamterene demonstrate that these drugs significantly increase the muscle magnesium content in patients on long term diuretic treatment for congestive heart failure and/or arterial hypertension--in addition to their well known positive effect on potassium balance.
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PMID:Intracellular magnesium loss after diuretic administration. 649 98

Ischaemic heart disease (IHD) is a major public health problem in most industrialised countries. In the death rates from IHD, marked differences exist between various countries and also between different areas of individual countries. Unfavourable dietary factors appear to play an important role in the aetiology of IHD, and thus differences in dietary habits and the quality of food may be mainly responsible for the geographic differences in the prevalence of IHD. The present liberal use of salt as well as the refining and other industrial processing of food increase the content of sodium and decrease the content of potassium and magnesium in the diet. The high intake of sodium and the inadequately low levels of potassium and magnesium in the diet predispose to the development of arterial hypertension. Since arterial hypertension is a major risk factor of IHD, the distorted electrolyte composition of our present diet can be considered an important aetiological factor of this disease. To decrease the body burden of sodium, diuretic agents are frequently used. Unfortunately, in the presence of the relatively low content of potassium and magnesium in the diet, the diuretic-induced increases in the excretion of these electrolytes commonly decrease the potassium and magnesium levels in the body. The falls in potassium and magnesium may increase the death rate from IHD by predisposing the heart to fatal arrhythmias, and also by other mechanisms. The likelihood of magnesium deficiency also appears to be influenced by the area of residence. The higher-than-average death rates from IHD in the so-called North Karelia area in eastern Finland and in some other areas with exceptionally high death rates from this disease may be at least partly due to the very low levels of magnesium in the soil and drinking water. It can be concluded that electrolyte disturbances have important implications in the aetiology and pathogenesis of IHD.
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PMID:Ischaemic heart disease. An epidemiological perspective with special reference to electrolytes. 649 99

Clinical and experimental data demonstrate that hormonal factors are involved in magnesium regulation. It is possible that the parathyroid hormone could play an important role in the maintenance of normal calcium and magnesium concentrations. The action of other hormones in magnesium metabolism appears to be an indirect response to factors such as calcium concentration or changes in volume. Alterations of the magnesium concentrations are important for the intracellular potassium, sodium and calcium content. Magnesium deficiency appears to lower intracellular potassium and to increase intracellular sodium and calcium concentrations. Therefore, magnesium is essential to avoid cardiovascular diseases (acute myocardial infarction, arrhythmias, hypertension) and to restore cellular potassium concentrations.
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PMID:Magnesium, potassium and hormonal regulation. 653 34


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