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Int J Cardiol. 1997 Dec 31;62 Suppl 2:S17-22.

Pharmacologic treatment of atherosclerosis: beyond lipid-lowering therapy.

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CNRS, Université René Descartes, Paris, France.


Increased proliferation of intimal smooth muscle cells (SMCs), resulting in myointimal hyperplasia and luminal narrowing, is a characteristic of the early phase of atherogenesis. Since agents that reduce this process could potentially be considered as alternatives to lipid-lowering therapy in the prevention/treatment of atherosclerosis, it is of interest to elucidate the mechanisms involved in myointimal proliferation. This review focuses on the main mechanisms that control vascular SMC reactivity/proliferation with particular reference to spontaneously hypertensive rat-derived arterial cells, which exhibit exaggerated growth and hyperresponsiveness to stimuli compared with cells from normotensive Wistar-Kyoto rats. In view of the fact that overall cell reactivity is under the control of free Ca2+ ions, the beneficial effects of calcium antagonists on the prevention/treatment of atherosclerosis are discussed. In particular, the mechanisms whereby amlodipine--a vascular selective inhibitor of inward Ca2+ current carried by the L-type Ca2+ channels--can affect cell growth and exhibit antiatherogenic properties are reviewed.

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