Role of magnesium and potassium in the pathogenesis of arteriosclerosis.
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)
D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology* / Q000378:metabolism; D001792:Blood Platelets / Q000378:metabolism; D002114:Calcinosis / Q000209:etiology; D003094:Collagen / Q000378:metabolism; D003920:Diabetes Mellitus / Q000378:metabolism; D004032:Diet; D004549:Elastin / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000209:etiology; D050356:Lipid Metabolism; D008074:Lipoproteins / Q000378:metabolism; D008274:Magnesium / Q000378:metabolism*; D008275:Magnesium Deficiency / Q000150:complications; D009131:Muscle, Smooth, Vascular / Q000378:metabolism; D011188:Potassium / Q000378:metabolism*; D011191:Potassium Deficiency / Q000150:complications; D051381:Rats; D013927:Thrombosis / Q000209:etiology
D008074:Lipoproteins; D003094:Collagen; D004549:Elastin; D008274:Magnesium; D011188:Potassium