In studies concerning risk factors for
cardiovascular diseases, a number of reports have emphasized the influence of
lipids, but the role of dietary minerals other than
sodium has been less studied. However, epidemiological studies have suggested that dietary intake of
magnesium and
potassium may be involved in such pathogenesis. Studies of the influence of
magnesium deficiency on
arteriosclerosis include its effect on the initial lesion, altered metabolism of
elastin, proliferation of
collagen, calcification, lipid metabolism, platelet aggregation and
hypertension.
Magnesium and
potassium metabolism are closely related and
magnesium is required for maintaining the level of cellular
potassium. As a consequence,
magnesium and
potassium deficiency frequently occur together and
potassium deficiency may be an aggravating factor in pathogenesis. The development of the initial lesion in the arterial wall may be facilitated by loss of cellular
magnesium and
potassium. Experimental
magnesium deficiency induces arterial damage, a loss of
magnesium and
potassium and an increase in the
calcium and
sodium content of the cell. Experimental models that have been used to produce cardiovascular lesions induce similar changes and losses of major intracellular
cations may affect the main metabolic processes of the cell. This report summarizes the experimental evidence that
magnesium deficiency may affect several different stages involved in
arteriosclerosis and that
potassium deficiency may exacerbate this.
Magnesium deficiency results in
vascular calcification. Experiments indicate that
elastin is the site of the initial calcification and the metabolism of
elastin is altered. This vascular lesion then brings about an increase in the
collagen content of the wall. Low
magnesium status could probably affect this process by slowing
collagen resorption and lead to an irreversible accumulation of connective tissue. Results showing a different distribution of the various types of
lipoprotein during experimental
magnesium deficiency strongly suggest that
lipid exchange between the vessel walls and blood can be modified. Severe
magnesium deficiency in weanling rats produces a marked
hypertriglyceridemia, a decrease in the percentage of
cholesterol transported by HDL
lipoprotein and a reduction in LCAT activity. The decreased clearance of circulatory
triglycerides appears to be the major mechanism contributing to
hyperlipemia.
Magnesium deficiency could therefore contribute to accumulation of vascular
lipid.
Magnesium and
potassium depletion have also been reported in diabetes and the vascular implications of this should be considered.(ABSTRACT TRUNCATED AT 400 WORDS)