<H4>The use of oral magnesium in mild-to-moderate congestive heart failure </h4><I>
Congestive Heart Failure (USA), 1997, 3/2 (21-24)</I><BR>
Magnesium has been shown to increase cardiac output and low serum magnesium concentrations are associated with frequent arrhythmias and higher mortality in patients with HF. We investigated the use of oral magnesium oxide in decreasing the morbidity and mortality in patients with mild-to- moderate HF. Oral magnesium oxide or placebo was given to 10 patients with NYHA Class II and III HF in a double-blind manner. In monthly follow-up visits, we measured magnesium levels, Euroquol quality of life values, mean arterial pressures, heart rates, and feet walked in 6 minutes. The mean arterial pressure increased an average of 5.3 mm Hg in the magnesium oxide group and decreased an average of 0.67 mm Hg in the placebo group (p = 0.0174). In addition, the heart rate decreased in the patients receiving magnesium oxide, and increased in the patients receiving placebo (p=0.0994). In each group, the NYHA Class decreased, while the Euroquol scale values and feet walked in 6 minutes increased. Due to the small number of patients enrolled, studies with greater numbers of patients that analyze additional oral formulations of magnesium would be beneficial. In addition enrolling HF patients in outpatient programs would be helpful.
<H4>Magnesium deficiency produces spasms of coronary arteries: Relationship to etiology of sudden death ischemic heart disease </h4><I>
SCIENCE (USA), 1980, 208/4440 (198-200)</I><BR>
Isolated coronary arteries from dogs were incubated in Krebs-Ringer bicarbonate solution and exposed to normal, high, and low concentrations of magnesium in the medium. Sudden withdrawal of magnesium from the medium increased whereas high concentrations of magnesium decreased the basal tension of the arteries. The absence of magnesium in the medium significantly potentiated the contractile responses of both small and large coronary arteries to norepinephrine, acetylcholine, serotonin, angiotensin, and potassium. These data support the hypothesis that magnesium deficiency, associated with sudden death ischemic heart disease, produces coronary arterial spasm.
<H4>Overview--suppression effect of essential trace elements on arteriosclerotic development and it's mechanism</h4><I>
Saito N Nippon Rinsho (JAPAN) Jan 1996, 54 (1) p59-66</I><BR>
It is known that the peroxidation of LDL is a trigger for developing arteriosclerosis. The oxidized LDL is produced by either oxidative stress or a few oxidant. Selenium decreased in serum and some organs of stroke-prone spontaneously hypertensive rats (SHRSP), which is a cofactor of glutamine peroxidase. Serum magnesium decreased in patients with diabetes mellitus, with ischemic heart disease, with essential hypertension and with cerebral vascular lesions. Calcium to magnesium ratio was higher in some organs of SHRSP as compared to Wistar Kyoto rats (WKY). These changes accelerated vascular lesions in SHRSP. (21 Refs.)
<H4>Relationship of magnesium intake and other dietary factors to blood pressure: the Honolulu heart study</h4><I>
Am J Clin Nutr (UNITED STATES) Feb 1987, 45 (2) p469-75</I><BR>
Associations between blood pressure and intakes of 61 dietary variables assessed by 24-h recall method were investigated in 615 men of Japanese ancestry living in Hawaii who had no history of cardiovascular disease or treated hypertension. Magnesium, calcium, phosphorus, potassium, fiber, vegetable protein, starch, vitamin C, and vitamin D intakes were significant variables that showed inverse associations with blood pressure in univariate and a multivariate analyses. Magnesium had the strongest association with blood pressure, which supports recent interest in its relation to blood pressure. Nevertheless, it was not possible to separate the effect of magnesium from that of other variables because of the problem of high intercorrelation among many nutrients. While recommendations based upon cross-sectional studies must be viewed cautiously, these results suggest that foods such as vegetables, fruits, whole grains, and low-fat dairy items are major sources of nutrients that may be protective against hypertension.
<H4>Hypertension, diabetes mellitus, and insulin resistance: the role of intracellular magnesium </h4><I>
Am J Hypertens (UNITED STATES) Mar 1997, 10 (3) p346-55</I><BR>
Magnesium is one of the most abundant ions present in living cells and its plasma concentration is remarkably constant in healthy subjects. Plasma and intracellular magnesium concentrations are tightly regulated by several factors. Among them, insulin seems to be one of the most important. In fact, in vitro and in vivo studies have demonstrated that insulin may modulate the shift of magnesium from extracellular to intracellular space. Intracellular magnesium concentration has also been shown to be effective on modulating insulin action (mainly oxidative glucose metabolism), offset calcium-related excitation-contraction coupling, and decrease smooth cell responsiveness to depolarizing stimuli, by stimulating Ca2+-dependent K+ channels. A poor intracellular magnesium concentration, as found in non-insulin-dependent diabetes mellitus (NIDDM) and in hypertensive (HP) patients, may result in a defective tyrosine-kinase activity at the insulin receptor level and exaggerated intracellular calcium concentration. Both events are responsible for the impairment in insulin action and a worsening of insulin resistance in non-insulin-dependent diabetic and hypertensive patients. By contrast, in NIDDM patients daily magnesium administration, restoring a more appropriate intracellular magnesium concentration, contributes to improve insulin-mediated glucose uptake. Similarly, in HP patients magnesium administration may be useful in decreasing arterial blood pressure and improving insulin-mediated glucose uptake. The benefits deriving from daily magnesium supplementation in NIDDM and HP patients are further supported by epidemiological studies showing that high daily magnesium intake to be predictive of a lower incidence of NIDDM and HP.
In conclusion, a growing body of studies suggest that intracellular magnesium may play a key role on modulating insulin-mediated glucose uptake and vascular tone. We further suggest that a reduced intracellular magnesium concentration might be the missing link helping to explain the epidemiological association between NIDDM and hypertension. (74 Refs.)
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