Sowers J R
Division of Endocrinology and Hypertension, Wayne State University Medical School, Detroit, MI 48201.
Am J Kidney Dis. 1990 Oct;16(4 Suppl 1):3-9.
Several chemical classes of calcium channel blockers (CCBs) inhibit atherosclerotic lesion formation in rabbit models by reduction of calcium, lipid, and matrix accumulation in the arterial wall. The mechanisms of these antiatherogenic effects are under investigation. Smooth muscle cells and macrophages, which synthesize matrix products and accumulate intracellular lipids, play a central role in lesion formation. Smooth muscle cell hyperplasia, with intracellular and functional changes, is common to both atherosclerosis and hypertension. The antiatherogenic properties of CCBs may be related in part to the protection of arterial cells from calcium overload through inhibition of calcium flux across voltage-regulated ion channels. CCBs may also inhibit cell migration, influence the uptake and catabolism of lipoproteins, alter smooth muscle matrix synthesis, and promote the depletion of intracellular cholesteryl ester stores. It appears that CCBs may inhibit the development of atherosclerotic lesions by two sets of mechanisms: alteration of lipid metabolism in smooth muscle cells and regulation of calcium-initiated or -accelerated intracellular processes.
