Abstract
Cell proliferation is now recognized as a common feature of the vascular response to injury characteristic of both hypertension and atherosclerosis. Our concepts of the role of proliferation in the underlying mechanisms for each disease, however, have been entirely different.
Current concepts about atherosclerosis began with the work of Virchow. He recognized the presence of cell proliferation in atherosclerosis over a century ago but viewed the cellular events as reactive rather than etiologic (1). This view has changed over the last two decades. With the development of the electron microscope, pathologists were able to identify the smooth muscle cell as the characteristic cell of the atherosclerotic plaque. A number of manipulations, including removal of the endothelium and exposure of the animals to hyperlipemia were shown to result in smooth muscle proliferation. These studies in animals and in humans support the idea that the initial step in lesion formation, prior to increase in intimal lipids, is the formation of focal masses of smooth cells in the intima (2-4). For at least some investigators, smooth muscle proliferation is now seen as the fundamental, etiologic event in atherosclerosis.
Our concepts of the role of smooth muscle cell proliferation in hypertension are more recent. Most research in hypertension has emphasized the role of physiologic controls of cell contractility or cell volume (5, 6). The pathology of the disease, much as with Virchow's early view of atherosclerosis, has been thought of as a reactive, rather than a causal part of the process. There is, however, general agreement that chronic hypertension is associated with vessel narrowing, presumably resulting from a thickening of the vessel wall (7-10). This “structural change” can account for a portion of the increased resistance to flow even when the vascular bed is chemically relaxed.
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