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The relationship between experimental magnesium deficiency and blood pressure is complex and still the subject of much debate. The effect of Mg deficiency and blood pressure in Wistar rats receiving a Mg deficient diet (0.080 g/kg) for 40 weeks was examined. Deficient rats, when compared to controls, showed an initial transitory phase of hypotension, followed by normalization of blood pressure and then hypertension beginning after 15 weeks on the deficient diet. During the whole experimental period, heart rate was significantly increased in deficient rats as compared to controls. The fact that hypotension resulting from Mg deficiency of short duration can be inhibited by antihistamines and by indomethacin suggests that various mediators seen during the inflammatory period of Mg deficiency could be involved. Mg deficiency of long duration was accompanied by hypertension. When Mg-deficient rats received the control diet for a period of 3 weeks, Mg supplementation only partially corrected the hypertension. The hypertension was not a consequence of stimulation of the renin-angiotensin system since the plasma renin activity was not modified and ACE activity was reduced. These deficient rats showed a significantly lower vasopressor response to noradrenaline than control rats. Several factors such as increase in collagen, changes in elastin and arterial elasticity, total lipid content, and calcifications may account for the hyporesponsiveness to contractile agonists.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Magnesium and blood pressure. I. Animal studies. 139 7

A large body of evidence demonstrates the prevalence and adverse clinical consequences of magnesium deficiency in patients with diabetes mellitus. It would be prudent for physicians who treat these patients to consider magnesium deficiency as a contributing factor in many diabetic complications and in exacerbation of the disease itself. Repletion of the deficiency or prophylactic supplementation with oral magnesium may help avoid or ameliorate such complications as arrhythmias, hypertension, and sudden cardiac death and may even improve the course of the diabetic condition.
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PMID:Magnesium deficiency and diabetes mellitus. Causes and effects. 140 73

Magnesium deficiency is common but difficult to diagnose and to assess in clinical practice. The use of a magnesium loading test was therefore evaluated to diagnose magnesium deficiency in 661 hospitalized patients with medical conditions assumed to interfere with magnesium uptake and excretion. Thirty millimoles of magnesium sulphate were administered intravenously during 8 h as a loading test and related to the urinary excretion in the following 24 h. A group of 30 patients without any known predisposition for magnesium deficiency and a group of 27 healthy volunteers served as controls. The mean (with 95% confidence interval) magnesium retention was 4 (-2-10)% in the control group of patients and 3 (-2-8)% in healthy subjects. A significantly higher retention was observed in all the groups of the patients: atrial fibrillation 18 (11-25)%, other arrhythmias 18 (11-24)%, hypertension 27 (20-33)%, coronary artery disease 25 (20-30)%, congestive heart failure 31 (26-37)%, cerebrovascular events 38 (24-51)%, gastrointestinal disorders 22 (14-29)%, diabetes mellitus 16 (9-22)%, and alcoholics 33 (29-36)%. The percentage of patients with a retention greater than mean + 2 SD of the two control groups varied between 22% and 54% among the different patient groups. The mean serum magnesium among the patient groups was similar to the control group of patients, except for the alcoholics, hypertensives and young healthy controls, who had significantly reduced levels. Magnesium retention was significantly correlated to age and renal function, and among the alcoholics negatively correlated to serum magnesium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Magnesium deficiency diagnosed by an intravenous loading test. 143 10

We have previously reported that antioxidant drug intervention protects against magnesium deficiency-induced myocardial lesions. In the present study, Golden Syrian male hamsters were fed either a magnesium-deficient diet or a magnesium-supplemented diet. Animals from each group received sulfhydryl-containing angiotensin converting enzyme inhibitors: captopril, epi-captopril (a stereoisomer of captopril), and zofenopril* (arginine blend of zofenopril containing a free SH group); another group of animals received the non-sulfhydryl-containing angiotensin converting enzyme inhibitor enalaprilat. The animals were killed after 14 days, and their hearts were isolated for morphological and morphometric analyses. Hematoxylin and eosin-stained sections were examined by a computer image analysis system for a morphometric determination of the severity of myocardial injury. Captopril reduced both the density of lesions, from 0.32 to 0.08 lesions/(mm2) (p less than 0.01), and the area fraction of lesions, from 7.42 x 10(-4) to 2.03 x 10(-4) lesion area/(mm2) (p less than 0.01), as well as the degree of inflammatory infiltration around the blood vessels. Epi-captopril and zofenopril* were virtually equipotent to captopril, but enalaprilat afforded only slight (nonsignificant) protection. These results indicate that a significant component of the protective effect of captopril in this model was attributable to its sulfhydryl moiety, rather than solely due to the inhibition of the angiotensin converting enzyme. These data further support our previous findings of possible free radical participation in cardiomyopathy due to magnesium deficiency.
Hypertension 1991 Aug
PMID:Captopril protects against myocardial injury induced by magnesium deficiency. 165 86

The overall importance of nutrition to favorable perinatal outcome is only beginning to be fully appreciated. Although nutritional status can be linked to such things as socioeconomic class and education, it is nutrition directly that exerts a biologic effect. This review has attempted to look at three elements and their relationship to maternal and fetal outcome. At the present time, there does not seem to be a role for routine magnesium supplementation during pregnancy. Magnesium deficiency, as an isolated nutritional deficiency, is rare, and the evidence is, at best, weak that magnesium supplementation reduces the risk of poor perinatal outcome. Zinc deficiency is also a very rare isolated nutritional finding. Our ability to measure zinc accurately, be it in leukocytes or serum, is improving, but the routine use of zinc supplements during pregnancy cannot be recommended at this time. It may be that zinc will be a useful diagnostic marker, rather than a therapeutic intervention. There is substantial evidence that the average American diet does not contain sufficient calcium. An expansive literature continues to grow in the areas of calcium and colon cancer, calcium and breast cancer, calcium and hypertension, and calcium and osteoporosis. Is it possible that our susceptibilities to these problems begin in utero? Obviously, the answer is unknown. What is known is that supplemental calcium to some degree is needed in the diets of most Americans and in about two thirds of pregnant women. Calcium supplementation seems to affect blood pressure favorably and, pending confirmation with larger trials, may significantly reduce prematurity and preeclampsia risk, thus improving perinatal outcome for a large number of our high-risk patients.
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PMID:Calcium, magnesium, and zinc supplementation and perinatal outcome. 186 34

The role of dietary calcium and magnesium in the development of hypertension was studied in nine groups, each consisting of nine spontaneously hypertensive rats aged 8-31 weeks. The animals were fed AIN 76A semi-purified diets varying in calcium (0.075, 0.5 and 2.5%) and magnesium (0.01, 0.05 and 0.75%) concentrations according to a 3 x 3 factorial design. Dietary calcium and systolic blood pressure were inversely related, significantly (P less than 0.05) after 12 weeks. Total and ultrafilterable serum calcium concentrations were also significantly negatively correlated with blood pressure (r = -0.46; P = 0.001 and r = -0.57; P = 0.001, respectively). Repeated measures analysis of variance indicated that dietary magnesium had no effect on systolic blood pressure, and no calcium x magnesium interaction on blood pressure was observed. Signs of magnesium deficiency, calcium deposits in the kidneys, and histological lesions were observed in groups on a high-calcium diet receiving normal and low levels of magnesium. Thus a lowering of blood pressure by calcium supplementation, without concomitant magnesium supplementation, was accompanied by biochemical and histological abnormalities in this animal model.
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PMID:Association of magnesium deficiency with the blood pressure-lowering effects of calcium. 216 Apr 89

Serum and erythrocyte magnesium concentrations (S-Mg, E-Mg) were measured in 122 junior high school students followed up for two years from 12 to 14 years of age, and the relationship to blood pressure and a family history of hypertension were investigated. The subjects who had high S-Mg and E-Mg levels at the first examination two years prior tended to show high levels after this follow-up. There were significant positive correlations between two intraindividual values of S-Mg and E-Mg. A similar tendency was found for blood pressure. Tracking phenomena were observed with these measures. The subjects who had high E-Mg levels at the first examination showed no blood pressure elevation during the two-year period. The subjects with a family history of hypertension [FH(+)] showed a higher degree of blood pressure rise during two years than those with no family history [FH(-)], with a significant difference in systolic blood pressure at the age of 14. E-Mg tended to be lower in the FH(+) group than in the FH(-) group with a significant difference in 14-year-old girls. These results suggest that a hereditary predisposition to hypertension is related to magnesium metabolism and that intracellular magnesium deficiency may influence blood pressure elevation in the FH(+) children.
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PMID:Relation of serum and erythrocyte magnesium levels to blood pressure and a family history of hypertension. A follow-up study in Japanese children, 12-14 years old. 233 46

Hypertension is a complex, heterogeneous disorder of which the exact etiology is unknown. The difficulty in ascribing an independent role to a single dietary constituent in blood pressure regulation may be due to interactions among nutrients which influence blood pressure. The effect of any one nutrient, particularly magnesium, on hypertension should be considered within the context of overall nutrition in each patient. Clinical, experimental and epidemiologic studies support the role of magnesium in hypertension, whereas a few studies negate this role. Magnesium ions are important in arterial smooth muscle contraction. Since magnesium is found mainly at the inner surface of the cell membranes, it could play a role in cell membrane permeability for sodium and calcium which is important in the etiopathogenesis of hypertension. Magnesium deficiency can predispose to increased contractility of the arteries and its excess can modulate smooth muscle contractility caused by bradykinin, angiotensin II, serotonin, prostaglandins and catecholamines. Magnesium therapy can prevent the development of resistant hypertension and arrhythmias in hypertensives with diuretic-induced hypomagnesemia. It might also reduce blood pressure at least up to 10/5 mm Hg provided adequate magnesium salts are given for an adequate period of time. In view of the still ill defined role of magnesium in hypertension, magnesium supplementation is advised only to those hypertensives who are receiving diuretics and develop resistant hypertension or who have frank magnesium deficiency. A diet rich in magnesium may be used for prevention of hypertension in predisposed communities because of the other advantages of such a diet in prevention.
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PMID:Magnesium metabolism in essential hypertension. 267 48

7.2 per cent of babies born in England and Wales in 1986 had birthweights below 2,500 g. Low birthweight and hypertension are associated. European trials have reported that oral supplementation with physiological amounts of magnesium during pregnancy reduces pregnancy hypertension and also miscarriage, preterm birth and fetal growth retardation. Magnesium deficiency causes hypertension and low birthweight in animals. In humans deficiency of thiamin and other B vitamins has also been reported to cause pregnancy hypertension and low birthweight. Magnesium and B vitamins are essential for the same biochemical reactions in energy metabolism. There is evidence that magnesium consumption of substantial numbers of women in Europe and North America is too low to support a healthy pregnancy. Magnesium and thiamin are lost in processing many foods. British trials of magnesium supplementation are advocated. It is suggested that more attention should be given to magnesium in nutritional advice.
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PMID:Magnesium and other nutrient deficiencies as possible causes of hypertension and low birthweight. 307

Serum and erythrocyte magnesium concentrations (S-Mg, E-Mg) were measured in 380 Japanese junior high school students, and the relationship to blood pressure and a family history of hypertension were studied. Systolic blood pressure was higher in the subjects with a positive family history of hypertension [FH(+)] than in those with a negative family history [FH(-)], whereas E-Mg was lower in the FH(+) group than in the FH(-) group with a significant different in boys. Furthermore, in the FH(+) group, systolic blood pressure was significantly higher in the subjects with lower S-Mg and E-Mg than in those with higher S-Mg and E-Mg. In the FH(-) group, however, no difference was observed in blood pressure levels between the two subgroups. These findings suggest that magnesium deficiency is partially responsible for a rise of blood pressure in the FH(+) children, and that a genetic predisposition of hypertension may be closely related to magnesium metabolism.
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PMID:Serum and erythrocyte magnesium levels in junior high school students: relation to blood pressure and a family history of hypertension. 324 81


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