Magnesium and cardiovascular system
http://www.jle.com/e-docs/00/04/59/7E/article.phtml "...Impact of magnesium on endothelial function
The vascular endothelium is an active paracrine, endocrine and autocrine organ, which plays a critical role in vascular homeostasis by secreting several mediators regulating vessel tone and diameter, coagulation factors, vascular inflammation, cell proliferation and migration, platelet and leukocyte interaction and activity and thrombus formation [66-73]. Endothelial dysfunction is therefore recognized as a major factor in the development of atherosclerosis, hypertension, and heart failure. Vascular endothelial dysfunction is an independent risk factor for cardiovascular events, and provides important prognostic data in addition to the classic cardiovascular risk factors and may be a “crystal ball prediction for enhanced cardiovascular risk” [74].
Shechter et al. [75] recently demonstrated that endothelial function is significantly correlated to intracellular magnesium levels, measured in sublingual epithelial cells, in CAD patients and oral magnesium 30 mmol/day (total magnesium 730 mg/day) for 6 months significantly increased intracellular magnesium compared to placebo. In addition themagnesium therapy resulted in a significant improvement in endothelial function, associated with improvement in exercise duration, exercise-induced chest pain and exercised-induced cardiac arrhythmias. Pearson et al. [76] demonstrated that hypomagnesemia selectively impaired the release of nitric oxide (NO) from coronary endothelium in a canine model. Paravicini et al. [77] demonstrated in a model of hypomagnesemia that blood pressure significantly increased in low intracellular magnesium levels compared with normal-high intracellular magnesium levels. The low intracellular magnesium levels were associated with impaired endothelial function together with decreased plasma nitrate levels and endothelial NO synthase expression when compared with normal-high intracellular magnesium levels. Because NO is a potent endogenous nitrovasodilator and inhibitor of platelet aggregation and adhesion, hypomagnesemia may promote vasoconstriction and coronary thrombosis in hypomagnesemic states. Endothelial cells actively contribute to inflammation in magnesium deficiency states. Magnesium intake is inversely associated with markers of systemic inflammation and endothelial dysfunction in healthy [26] and postmenopausal women [27]. .....
Conclusion:
Magnesium plays a vital role in many cellular processes. Magnesium is essential for a number of metabolic activities since it is associated with a variety of enzymes which control carbohydrate, fat, protein end electrolyte metabolism. Several hundred enzymes, directly or indirectly, are dependent on magnesium. Most important among these enzymes are those which hydrolyze and transfer phosphate groups, including enzymes that are concerned with reactions involving energy production and ATP. Magnesium deficiency, or reduction in the dietary intake of magnesium, plays an important role in the etiology of diabetes and numerous cardiovascular diseases including thrombosis, atherosclerosis, ischemic heart disease, myocardial infarction, hypertension, cardiac arrhythmias and CHF in humans.
Magnesium deficiency may lead to reduced energetic metabolite production and the sense of fatigue and/or “chronic fatigue syndrome”. Modern life styles and the Western industrial diet have enhanced the reduction of magnesium in our food, which contributes to marginal or absolute magnesium deficiency. The magnesium deficiency is mostly evidenced in the elderly population, those with myocardial infarction and/or CHF, diabetics, patients with chronic airway obstruction, pre- or toxemia of pregnancy, in post transplantation patients (especially in heart transplantation), patients with malignancies who receive cytotoxic chemical therapy, in competitive athletes and in metabolic syndrome patients.
It should be noted that magnesium deficiency can easily be treated by magnesium supplementation if we are aware of the situation. The best recommendation is to increase consumption of magnesium-rich food. However, since magnesium deficiency is hard to treat only by increase consuming high-magnesium food products, it is recommended to take magnesium supplements which officially and safely increase the magnesium in the body and correct the deficit.
There are theoretical potential benefits of magnesium supplementation as a cardioprotective agent in CAD patients, as well as promising results from previous work in animal and humans. Magnesium is an essential element in treating CAD patients, especially high-risk groups such as CAD patients with heart failure, the elderly and hospitalized patients with hypomagnesemia. Furthermore, magnesium therapy is indicated in life-threatening ventricular arrhythmias such as Torsades de Pointes and intractable ventricular tachycardia
Serum magnesium levels are not to be routinely advocated for screening subjects with magnesium deficiency, rather it should be highly suspicious unless proved otherwise.
It should be remembered that magnesium is neither a “panacea” nor a “wonder drug” which is aggressively pushed by the pharmaceutical industry. After all, it is a relatively simple nutrient, relatively non-expensive and easy to administer, with relatively few adverse events but also a “nutrient which is the sparkle of life” and an important life gatekeeper.”