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Effects of Mobile Phone Radio Frequency on the Structure and Function of the Normal Human Hemoglobin
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Evidence that increased reactive oxygen species are link between magnesium deficiency and hypertension
The relationship between high blood pressure and magnesium deficiency has been explored in several studies, producing conflicting evidence. A study published in the November 2002 issue of the Journal of Hypertension submits the hypothesis that insufficient levels of magnesium may lead to hypertension by increasing the formation of reactive oxygen species, harmful molecules that cause oxidative damage.
The University of Montreal researchers divided stroke-prone spontaneously hypertensive rats into three groups that received a control diet containing normal levels of magnesium, a magnesium-free diet and a high magnesium diet, and systolic blood pressure was measured each week for sixteen weeks. In a second experiment, stroke-prone spontaneously hypertensive rats received a control diet, a magnesium-free diet and a magnesium-free diet combined with Tempol, a superoxide dismutase mimetic for seven weeks. Superoxide dismutase is one of the antioxidants naturally produced in the body.
Rats in the low magnesium group experienced an exacerbation in the development of hypertension after five weeks, accompanied by a reduction in oxidative stress markers which increased rapidly after two weeks. The ability of blood vessels to dilate in response to acetylcholine was decreased in the low magnesium group compared to controls. Vessel wall hypertrophy was greater and vascular superoxide higher in the rats who received the magnesium deficient diet compared to those on the high magnesium diet. However, rats on magnesium-free diets receiving Tempol did not experience a progression of hypertension or the vascular changes seen in magnesium deficient rats who did not receive the antioxidant.
In an accompanying editorial, Richard D Bukoski writes that the research provides, "the first link between an essential dietary nutrient and the key molecular pathways involved in regulating vascular smooth muscle growth and structure." (Journal of Hypertension 2002, 20:2141-2143)