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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mineral elements sodium, potassium, calcium and magnesium play a central role in the normal regulation of blood pressure. In particular, these mineral elements have important interrelationships in the control of arterial resistance. These elements, especially sodium and potassium, also regulate the fluid balance of the body and, hence, influence the cardiac output. Evidence shows that the present levels of intake of mineral elements are not optimum for maintaining normal blood pressure but predispose to the development of arterial hypertension. Research results suggest that without sodium chloride (common salt) and other sodium compounds being added to the diet arterial hypertension would be virtually non existent. Moreover, blood pressure would not rise with age. In communities with a high consumption of added sodium, a high intake of potassium and, possibly, magnesium seem to protect against the development of arterial hypertension and the rise of blood pressure with age. A marked reduction of sodium intake is effective in treating even severe hypertension. A moderate restriction of sodium intake or an increase in potassium intake exert remarkable antihypertensive effects, at least in some hypertensive patients. Magnesium and possibly also calcium supplements may be effective in reducing blood pressure in some hypertensives. In hypertensive patients treated with drugs sodium restriction and potassium and magnesium supplementation enhance the therapeutic effect, reduce the number and dosage, and lessen the adverse effects of prescribed antihypertensive drugs. Hence, a fall in sodium consumption and increases in potassium and magnesium consumption are useful in preventing and treating arterial hypertension.
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PMID:Minerals and blood pressure. 193 Sep 21

Plasma and intra-erythrocytic magnesium concentrations were determined in 27 patients with pre-eclampsia and in 22 healthy pregnant women. In the pre-eclamptic women, the Mg2+ concentrations were measured before and after treatment with Mg2+ salts and after delivery. The plasma Mg2+ concentration was not significantly different in the pre-eclamptic and the healthy pregnant women. The intra-erythrocytic Mg2+ concentration before treatment with Mg2+ was significantly lower in the pre-eclamptic patients than in the healthy pregnant women [1.33 +/- 0.29 versus 1.01 +/- 0.16 mmol/l (means +/- s.d.); P less than 0.05] and increased after treatment with Mg2+ to 1.19 +/- 0.24 mmol/l. Lowered cellular Mg2+ concentrations in pre-eclampsia may contribute to the development of hypertension in this disorder.
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PMID:Plasma and intracellular Mg2+ concentrations in pre-eclampsia. 216 Apr 86

In the treatment of cardiac arrhythmias of varying genesis, an "observational study" in 1,160 patients showed that a high-dose oral magnesium preparation (Magnesium-Diasporal N 300 Granulat) was effective. In 82% of the patients observed, a dose of at least 300 mg magnesium/day produced good to very good results. Adverse effects of the drug were observed in only 1.6% of the patients. For all groups, the "success parameters" improved significantly. High-rate arrhythmias showed a better response to magnesium treatment than did low-rate arrhythmias, with a close correlation being found with the heart rate at the start of treatment. High-dose oral magnesium had a positive effect on concomitant hypertension. At a dosage of 300 mg treatment should be continued for at least 6 weeks.
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PMID:[High-dosage oral magnesium therapy in arrhythmias. Results of an observational study in 1.160 patients with arrhythmia]. 224 40

Magnesium may be important in the pathogenesis of coronary heart disease and sudden death. To study the role of magnesium, 400 high risk individuals were asked to volunteer either for a magnesium-rich diet (group A, 206) or for our usual diet (group B, 194) for 10 years in a randomized fashion. The age groups were between 25 and 63 years and the majority (374) of them were males. At entry to the study, age, sex, incidence of hypertension, diabetes, hypercholesterolemia, smoking, coronary disease and diuretic therapy were comparable. Dietary magnesium intake in group A (1,142 +/- 233 mg/day) was higher than in group B (418 +/- 105 mg/day). Total complications in group A (59; 28.6%) were significantly (p less than 0.001) less compared to group B (117; 60.3%). Sudden deaths were one and a half times more common in group B than in group A. Total mortality in group A (22; 10.7%) was significantly (p less than 0.01) less than in group B (34; 18.0%). A greater number of complications and increased mortality in group B subjects was consistent with a higher incidence of hypokalemia, hypomagnesemia and coronary risk factors in group B patients. Mean serum magnesium levels in group B participants were significantly (p less than 0.01) lowered compared to the mean magnesium level in group A participants who were administered the magnesium-rich diet. It is possible that increased intake of dietary magnesium in association with the general effects of a nutritious diet can offer protection against cardiovascular deaths among high-risk individuals predisposed to coronary heart disease.
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PMID:Effect of dietary magnesium supplementation in the prevention of coronary heart disease and sudden cardiac death. 224 95

Magnesium is an important ion in all living cells being a cofactor of many enzymes, especially those utilising high energy phosphate bounds. The relationship between insulin and magnesium has been recently studied. In particular it has been shown that magnesium plays the role of a second messenger for insulin action; on the other hand, insulin itself has been demonstrated to be an important regulatory factor of intracellular magnesium accumulation. Conditions associated with insulin resistance, such as hypertension or aging, are also associated with low intracellular magnesium contents. In diabetes mellitus, it is suggested that low intracellular magnesium levels result from both increased urinary losses and insulin resistance. The extent to which such a low intracellular magnesium content contributes to the development of macro- and microangiopathy remains to be established. A reduced intracellular magnesium content might contribute to the impaired insulin response and action which occurs in Type 2 (non-insulin-dependent) diabetes mellitus. Chronic magnesium supplementation can contribute to an improvement in both islet Beta-cell response and insulin action in non-insulin-dependent diabetic subjects.
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PMID:Magnesium and glucose homeostasis. 225 26

The placenta and the umbilical cord obtained from 18 women with pregnancy-induced hypertension were investigated by light microscopy. The umbilical artery was studied by electron microscopy. 10 placentae and umbilical cords from normal pregnancies served as controls. The study was performed as a double-blind randomized controlled study in which 11 women were allocated to magnesium and 7 to placebo treatment. The treatment comprised a 48-hour intravenous magnesium/placebo infusion followed by daily oral magnesium/placebo intake until one day after delivery. Magnesium supplement increased birth weight and placental weight significantly. Light microscopic study of the placentae and the umbilical cord arteries showed no difference between the three groups concerning the occurrence of infarctions, cytotrophoblastic hyperplasia, vasculo-syncytial membranes, basement membrane thickening, stromal fibrosis or intervillous fibrin. Ultrastructurally, the endothelial cells of the umbilical arteries from women with pregnancy-induced hypertension showed a significant increase in the amount of dilated endoplasmic reticulum and basal laminae thickness when all 18 cases were compared with the controls. There was no significant difference when the magnesium group, the placebo group and the control group were compared separately. The present study suggests that magnesium supplement has a beneficial effect on fetal growth in pregnancy-induced hypertension. With regard to the light and electron microscopic changes we were unable to demonstrate any significant difference between the magnesium, placebo and control groups.
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PMID:Magnesium supplement in pregnancy-induced hypertension. A clinicopathological study. 228 7

Accumulating experimental evidence suggests that natriuresis in response to intravascular volume expansion is promoted by an endogenous regulator of Na+,K+-adenosine triphosphatase (ATPase). Efforts to purify this substance by a number of laboratories have as yet been unsuccessful. The properties of partially purified inhibitors from plasma, urine, and tissue often fail to possess the characteristics thought to be consistent with those of a physiological regulator. These include potency (Ki of approximately 1 nM), reversibility of inhibition, specificity for Na+,K+-ATPase, and responsiveness to relevant physiological stimuli. Two rather different candidate substances, extracted from urine and hypothalamus, have been purified to a high degree. Neither is a peptide, and both are of low molecular weight and resistant to acid hydrolysis. The substance from urine is rather nonpolar and interacts with digoxin-specific antibodies, while that from hypothalamus is polar and does not appear to share epitopes with the cardiac glycosides. On the serosal surface of the toad urinary bladder, the hypothalamic substance causes a reversible inhibition of Na+ transport, inhibits rubidium uptake in red blood cells by acting on the membrane's exterior surface, inhibits binding of ouabain to purified Na+,K+-ATPase, and reversibly inhibits hydrolysis of adenosine 5'-triphosphate by the enzyme with a Ki of 1.4 nM. The hypothalamic inhibitor may be differentiated from ouabain by their respective ionic requirements for optimal inhibition of enzymatic activity, and although both ouabain and the hypothalamic inhibitor fix Na+,K+-ATPase in its E2 conformation, the hypothalamic inhibitor does not promote phosphorylation of the enzyme by inorganic phosphate in the presence of Mg2+. Ionic requirements for inhibition also differentiate the hypothalamic inhibitor from vanadate ion, as does the inhibitor's activity in the presence of norepinephrine. Further enzymological and physiological studies will be facilitated by structural characterizations of the inhibitory substances and by the availability of a method to measure their concentrations in physiological fluids.
Hypertension 1987 Apr
PMID:The search for a hypothalamic Na+,K+-ATPase inhibitor. 243 55

Evidence in vitro and in humans suggest that Mg2+ can alter systemic and renal vascular tone. However, the mechanism of these effects is not known. The role of vasodilator prostaglandin release and Ca2+ flux in Mg2+-induced changes in blood pressure and renal blood flow was studied in 10 normal subjects maintained on a fixed 80-mEq Na+ and K+ diet. Magnesium sulfate infused at 200 mg/hr for 3 hours reduced systolic and diastolic blood pressure within 1 hour (from 119 +/- 2 [SEM] to 109 +/- 4 mm Hg systolic; from 74 +/- 3 to 64 +/- 4 mm Hg diastolic; p less than 0.02). This hypotensive response was seen in all subjects and persisted for 3 hours. The pulse rate did not change, but renal blood flow (p-aminohippurate clearance) increased (from 902 +/- 78 to 1108 +/- 130 ml/min/1.73 m2; p less than 0.05). The Mg2+ infusion produced a significant increase in the excretion of the stable prostaglandin I2 (PGI2) metabolite 6-keto-PGF1 alpha (from 96 +/- 12 to 154 +/- 16 ng/g creatinine; p less than 0.01). In contrast, urinary PGE2 was not altered (328 +/- 75 vs 399 +/- 145 ng/g creatinine; p greater than 0.6). To evaluate the functional role of PGI2 release, the cyclooxygenase inhibitors indomethacin (75 mg) or ibuprofen (600 mg) were given before the Mg2+ infusion. Both cyclooxygenase blockers, given in doses that inhibited immunoreactive 6-keto-PGF1 alpha release, completely prevented the Mg2+-induced decline in blood pressure and increased renal blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1987 Apr
PMID:Evidence that prostacyclin mediates the vascular action of magnesium in humans. 243 56

We measured the ouabain- and bumetanide-resistant Na+ efflux in Mg2+-sucrose medium (passive Na+ leak) in erythrocytes from 30 normotensive controls and 72 essential hypertensive patients. The mean values (+/- SEM) of the rate constant of Na+ leak (kpNa) were not significantly different between normotensives and hypertensives. Nevertheless, using the 95% confidence limits of the kpNa (in 10(-3).h-1) in the normotensive group as a cut-off point, 7 (9.7%) essential hypertensives exhibited increased values (58.96 +/- 10.12) when compared with the other 65 patients (23.86 +/- 0.74). revealing increased passive Na+ permeability in the former (leak "+" hypertensives). Na+ fluxes depending on the Na+-K+ pump, outward Na+-K+ cotransport, and Na+-Li+ countertransport were also measured in fresh erythrocytes from the same 72 patients. Three of them (4.2%) exhibited decreased values of ouabain-sensitive Na+ efflux and 6 (8.3%) of bumetanide-sensitive Na+ efflux, while 8 patients (11.1%) showed increased values of Li+-stimulated Na+ efflux and, finally, 48 patients (59.7%) did not present any evident abnormality in these Na+ transport systems. No differences were observed between leak "+" hypertensives and the remaining 65 patients when both basal erythrocyte Na+ content and clinical parameters of hypertension were compared. However, Na+ efflux depending on the outward Na+-K+ cotransport was significantly higher in the leak "+" hypertensive subset (299.43 +/- 43.18 vs 181.52 +/- 10.76 mumol.(l cells.h)-1; P = 0.0078), suggesting a compensatory phenomenon. Enhancement of Na+ permeability detected in 3% to 16% of essential hypertensives may be implicated in the pathogenesis of primary hypertension.
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PMID:Abnormal erythrocyte sodium leak in a subset of essential hypertensive patients. 246 45

Magnesium therapy has been shown, by us, to attenuate monocrotaline (MCT)-induced pulmonary artery hypertension (PAH), right ventricular hypertrophy and pathological changes in the pulmonary vasculature in 75% of Sprague-Dawley rats. We studied Wistar rats to determine if there was a strain difference in response to MCT and magnesium therapy. Wistar rats were given 60 mg/kg of MCT and studied 3 weeks later, following a protocol similar to that for Sprague-Dawley rats. There was 100% mortality in Wistar rats weighing less than 230 g. The mortality rate in Sprague-Dawley rats of a similar weight range was significantly less (15%). With 40 mg/kg of MCT, Wistar rats developed pulmonary hypertension and right ventricular hypertrophy comparable to those seen in Sprague-Dawley rats administered 60 mg/kg MCT. The percent weight gain over a 3-week period was significantly higher in the Wistar control group than that in the Sprague-Dawley controls (61 vs. 39%; p less than 0.05). Oral magnesium therapy (magnesium aspartate HCl) attenuated pulmonary hypertension and right ventricular hypertrophy in 100% of the Wistar rats studied. A group of Sprague-Dawley rats was given 40 mg/kg of MCT and studied 3 weeks later. PAH and right ventricular hypertrophy in this group were not significantly different from the rats of the same strain injected with the higher dose of MCT. In conclusion, faster growing rats (Wistar) appear to be more sensitive to MCT. Both strains show a significant attenuation of cardiopulmonary changes induced by MCT when treated with oral magnesium.
Magnesium 1989
PMID:Strain differences in pulmonary hypertensive response to monocrotaline alkaloid and the beneficial effect of oral magnesium treatment. 252 10


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