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

A history of alcohol abuse associated with hypertension and chronic alcohol consumption is the leading cause of secondary cardiomyopathy. Both acute and chronic alcohol consumption precipitate arrhythmias. However moderate alcohol intake exerts a protective effect against coronary heart disease and stroke. Morbidity is lowest among light drinkers, slightly higher among lifelong abstainers and much higher among heavy drinkers. Magnesium deficiency is common among chronic alcoholics and frequent in Brazil. Magnesium therapy may have beneficial effects when there is excessive ethanol consumption.
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PMID:[Cardiovascular impact of alcoholism]. 748 61

Serum magnesium levels, as well as magnesium content of red blood cells and peripheral mononuclear cells, were examined in 31 pregnant women in their third trimester. Ten were preeclamptic; chronic hypertension was found in 10, and 11 were normotensive. Magnesium serum levels were 1.2 +/- 0.1, 1.2 +/- 0.1 and 1.3 +/- 0.1 mEq/l in the normotensives, chronic hypertensives and preeclamptics, respectively. Red blood cell magnesium concentration was 3.4 +/- 0.4, 3.7 +/- 0.7 and 3.5 +/- 0.5 mEq/l, and mononuclear magnesium content was 37.9 +/- 30.6, 27.6 +/- 15.9 and 30.2 +/- 25.7 fg/cell in the same groups, respectively. These changes were not statistically significant. The results do not support the hypothesis that magnesium deficiency is involved in the pathophysiology of preeclampsia.
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PMID:Mononuclear cell magnesium content remains unchanged in various hypertensive disorders of pregnancy. 785 4

Increased dietary fructose may produce insulin insensitivity and elevate blood pressure in rats. It is possible that the reduced magnesium content of the high-fructose commercial diet used in some studies may play a role in these abnormalities because it is known that magnesium deficiency can produce insulin insensitivity and increased angiotensin II action in humans. To study this, we maintained rats for 9 weeks on either a normal control diet, a standard high-fructose diet, or the same high-fructose diet supplemented with magnesium. Glucose uptake was assessed using a perfused rat hindquarter preparation sequentially with 0, 900, and 120,000 pmol/L of added insulin. Basal serum glucose, plasma insulin, and basal glucose uptake in the absence of insulin were similar among all three groups. However, insulin sensitivity, defined as glucose uptake in the presence of 900 pmol/L insulin minus basal, was depressed in the high-fructose compared with the control group (1.02 +/- 0.38 to 1.77 +/- 0.57 mumol/g per hour, P < .05). In contrast, the high-fructose group supplemented with normal magnesium had similar insulin sensitivity as the control group (2.09 +/- 0.69 mumol/g per hour). Total serum magnesium was reduced in the high-fructose group compared with control or high-fructose plus magnesium-supplemented groups. Blood pressure and fasting insulin levels were also lower in the magnesium-supplemented group. These results suggest that magnesium deficiency and not fructose ingestion per se leads to insulin insensitivity in skeletal muscle and changes in blood pressure.
Hypertension 1994 Jun
PMID:Dietary magnesium prevents fructose-induced insulin insensitivity in rats. 820 89

'Magnesium ischaemia' is a term used to denote the functional impairment of the ATP-dependent sodium/potassium and calcium pumps in the cell membranes and within the cell itself. The production of ATP and the functioning of these pumps is magnesium-dependent and is critically sensitive to acidosis. Zinc and iron deficiencies may secondarily impair these pumps and thus contribute to 'magnesium ischaemia' (as does acidosis). This term is two-dimensional at its simplest; it refers to a functional magnesium deficiency, whether actual or induced. It is argued that chronic acidosis is the most common inducing factor. This simple hypothesis can begin to unify diverse pathophysiologies: some spontaneous abortions, aspects of Type II and gestational diabetes and the curious observation that heroin addicts become diabetic. It can also unify clinical thinking about pregnancy-induced hypertension, pre-eclampsia/eclampsia and acute fatty liver of pregnancy, as well as the coagulopathy of pregnancy. It makes important predictions about perinatal morbidity and suggests that early supplementation might prevent much pregnancy-induced disease.
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PMID:The pathogenesis of eclampsia: the 'magnesium ischaemia' hypothesis. 839 28

Magnesium concentrations were measured in the serum of 159 pregnant women, 19 patients with severe, 64 with mild gestational hypertension and 76 with a normal pregnancy. Our data do not support the conclusion that magnesium deficiency is the primary cause of gestational hypertension.
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PMID:[Magnesium content of serum in pregnancy-induced hypertension]. 840 Sep 12

Evidence suggests that magnesium deficiency may play an important role in cardiovascular disease. In this study, we evaluated the effects of a magnesium infusion and dietary-induced isolated magnesium deficiency on the production of thromboxane and on angiotensin II-mediated aldosterone synthesis in normal human subjects. Because insulin resistance may be associated with altered blood pressure, we also measured insulin sensitivity using an intravenous glucose tolerance test with minimal model analysis in six subjects. The magnesium infusion reduced urinary thromboxane concentration and angiotensin II-induced plasma aldosterone levels. The low magnesium diet reduced both serum magnesium and intracellular free magnesium in red blood cells as determined by nuclear magnetic resonance (186 +/- 10 [SEM] to 127 +/- 9 mM, p < 0.01). Urinary thromboxane concentration measured by radioimmunoassay increased after magnesium deficiency. Similarly, angiotensin II-induced plasma aldosterone concentration increased after magnesium deficiency. Analysis showed that all subjects studied had a decrease in insulin sensitivity after magnesium deficiency (3.69 +/- 0.6 to 2.75 +/- 0.5 min-1 per microunit per milliliter x 10(-4), p < 0.03). We conclude that dietary-induced magnesium deficiency 1) increases thromboxane urinary concentration and 2) enhances angiotensin-induced aldosterone synthesis. These effects are associated with a decrease in insulin action, suggesting that magnesium deficiency may be a common factor associated with insulin resistance and vascular disease.
Hypertension 1993 Jun
PMID:Magnesium deficiency produces insulin resistance and increased thromboxane synthesis. 850 87

This study examines the effect of long-term magnesium-deficient diet on blood pressure and vascular reactivity in aged spontaneously hypertensive rats (SHR) with established hypertension. Thirty-one-week old male SHR received control (0.15 per cent magnesium) and magnesium-deficient (0.015 per cent magnesium) diets for 30 weeks. Systolic blood pressure was measured by tail-cuff method. At the end of the study, the heart, aorta and kidney were collected to measure total magnesium and calcium concentrations; the ex vivo effects of the different magnesium diets on vascular reactivity were examined in isolated aorta and in the isolated perfused mesenteric vascular bed. After 30 weeks, magnesium deficiency had no effect on systolic blood pressure and heart rate of SHR. The tissue concentrations of total magnesium in aorta, heart and kidney were not modified by magnesium deficient diet. Total calcium concentration was significantly higher in the heart of the SHR fed the magnesium-deficient diet (p < 0.01). The aortic responsiveness to contractile agents norepinephrine, endothelin-1, CaCl2 and KCl, and to vasorelaxant agents acetylcholine and isoproterenol were not modified by magnesium deficiency. The vasoconstrictor activity to norepinephrine, CaCl2 and KCl was significantly enhanced in the isolated perfused mesenteric vascular bed of magnesium-deficient SHR (p < 0.05). In conclusion, magnesium deficient diet fails to elevate blood pressure in aged SHR maintained on deficiency for 30 weeks despite an enhanced ex vivo vasoconstrictor activity.
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PMID:Magnesium deficiency increases vasoconstrictor activity without affecting blood pressure of aged spontaneously hypertensive rats. 936 31

Improving the action of insulin is a relatively new concept in therapy. It should, however, become more and more important because of the rapid expansion of the insulin resistance syndrome (including upper body adiposity, glucose intolerance, hypertension, dyslipidaemia, etc.) in industrialized countries and its dramatic consequences for public health. Insulin sensitivity can be improved by non-pharmacological means, essentially reduction of excessive body weight, promotion of regular physical activity and modification of dietary habits, as well as, possibly, cessation of smoking and correction of subclinical magnesium deficiency. Currently available pharmacological means mainly include the biguanide compound metformin and possibly anti-obesity agents, such as (d-) fenfluramine, fluoxetine and benfluorex. New compounds aiming at improving the action of insulin are in development, especially the thiazolidinedione derivatives (e.g. troglitazone), known as 'insulin sensitizers'. Treatment of insulin resistance may have important gynaecological applications, essentially in polycystic ovary syndrome and, possibly, after menopause. Hopefully, improving insulin sensitivity could ameliorate the cardiovascular prognosis of numerous individuals having some or all components of insulin resistance syndrome.
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PMID:Perspective in the treatment of insulin resistance. 940 22

A tendency for magnesium deficiency in patients with diabetes mellitus is well-established. Glucosuria-related hypermagnesiuria, nutritional factors and hyperinsulinaemia-related hypermagnesiuria all can contribute. The plasma magnesium level has been shown to be inversely related to insulin sensitivity. Magnesium supplementation improves insulin sensitivity as well as insulin secretion in patients with type 2 diabetes. Nevertheless, no beneficial effects of oral magnesium supplementation has been demonstrated on glycaemic control either in patients with diabetes type 1 or 2. Oral magnesium supplementation reduced the development of type 2 diabetes in predisposed rats. There are some indications that magnesium decreases blood pressure, but negative results have been observed in trials that were, however, not designed to test effect on blood pressure as primary parameter. Patients with (severe) retinopathy have a lower plasma magnesium level compared to patients without retinopathy and a prospective study has shown the plasma magnesium level to be inversely related to occurrence or progression of retinopathy. Further study on magnesium (supplementation) is warranted in the prevention of type 2 and of (progression of) retinopathy as well as a means to reduce high blood pressure.
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PMID:Magnesium in diabetes mellitus. 1021 82

A close relationship between magnesium and cardiovascular function has been reported; however, the effect of magnesium deficiency on autonomic cardiovascular regulation has not been clarified. We investigated the effect of magnesium deficiency on the autonomic regulation of oscillations of the R-R interval, arterial blood pressure (BP), and renal sympathetic nerve activity (RSNA) by using the maximum entropy method in conscious rats. Its effect on baroreflex control of RSNA and heart rate were also investigated with a logistic function curve. Mean BP in magnesium-deficient rats was higher than that in control rats (mean+/-SE, 114.0+/-4.3 versus 101.6+/-3.4 mm Hg; P<0.05), and urinary excretion of catecholamine was increased by 2.4-fold. The fraction of low-frequency oscillation of RSNA was reduced (31.7+/-0.9% versus 36.2+/-1.5%, P<0.05) and the correlation between low-frequency oscillations of BP and RSNA was weakened in magnesium-deficient rats. There was no difference in high-frequency oscillation of the R-R interval, which is related to vagal tone, whereas sympathetic tone became dominant (square root of low-frequency/high-frequency ratio of R-R interval, 1.00+/-0.05 versus 0.67+/-0.05, P<0.0001) in magnesium-deficient rats. The maximal gain in the BP-RSNA relation tended to be reduced in magnesium-deficient rats (-7.7+/-1.1% versus -12.2+/-1.9%/mm Hg, P=0. 07); however, that in the BP-heart rate relation was increased (-8. 1+/-0.7 versus -4.5+/-0.5 bpm/mm Hg, P<0.01). These results suggest that magnesium deficiency induces sympathetic excitation, which results in hypertension but attenuates the baroreflex-related response of sympathetic nerves, whereas magnesium deficiency enhances the sensitivity of the sinus node to autonomic regulation.
Hypertension 1999 Aug
PMID:Effect of magnesium deficiency on autonomic circulatory regulation in conscious rats. 1045 49


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