Arterial calcium metabolism, hypertension and arteriosclerosis

Recent research emphasizes the importance of calcium transport in smooth muscle in the etiology of essential hypertension. Mönckeberg's arteriosclerosis may be due to the deposition of such calcium in the media of the large arteries, made ischemic and necrotic by a decrease in adventitial blood supply, as well as a decrease in luminal endothelial and intimal permeability; and also aided by chemicals derived from fragmented elastic tissue. In atherosclerosis, rupture of the internal elastica causes smooth muscle to migrate into plaques which become cholesterol- and lipid-filled and finally calcified. Endothelial cracks or ulcers cause the deposition of platelets which have internal calcium transport mechanisms similar to those of smooth muscle and so, on deterioration, contribute to the deposition of calcium. In arterioles, where there is no or minimal adventitial blood supply, where smooth muscle contraction counteracts lateral stretch and hence rupture of the internal elastica and where pressures are lower, plasmatic protein influx, as well as necrosis, causes hyalinization and connective tissue scarring rather than calcium deposition. In other words, calcification of blood vessels may occur because of the precipitation of this ion from the sources already mentioned, as well as because of a possible attraction of the ion into the lesion from the blood stream. If it is precipitated as calcium apatite, the lesion can resemble bone. In veins and in the pulmonary artery, calcium deposition is rare except when there is increased pressure or thrombosis.