Recent advances in molecular pathology. The effects of hypertension on the arterial wall.
Hypertension is a major risk factor for clinically significant atherosclerotic vascular disease in Western Society, although the link between these conditions remains very poorly understood. Recent studies which are reviewed here have demonstrated that major arterial intimal and medial abnormalities occur as a result of hypertension. These include functional changes in endothelial permeability as well as alterations in the endothelial cells themselves with an increase in their turnover and number and distinct changes in morphology. However, endothelial cell loss leading to denudation of the arterial intimal surface appears to be relatively uncommon. Intimal and medial thickening are consistent features of hypertension and result from increases in both cellular and extracellular components. The cells accumulating in the subendothelial space appear to be of both blood-borne and medial origins, although their complete characterization has not been performed as yet. The adherence of blood cells to the endothelial surface appears to be promoted by the presence of hypertension along with their increased entry into the intima through endothelial cell junctions. Medial thickening with hypertension is attributable primarily to increased smooth muscle cell mass, although enhanced deposition of collagen and elastin plays a contributory role. Recent data would indicate that smooth muscle cell hypertrophy rather than hyperplasia is primarily responsible for the greater smooth muscle mass with hypertension. Although elevated DNA content of hypertensive arteries has been demonstrated, such changes may be secondary to a marked increase in cells showing nuclear polyploidy. Prolonged normalization of blood pressure in hypertensive animals can produce considerable regression of arterial changes toward the control state. The changes appear more marked with respect to the cellular rather than the extracellular abnormalities induced by hypertension. In man, little is known about the effects of antihypertensive therapy on the vasculature itself, although clinical complications related to both hemorrhagic or thrombotic strokes are clearly reduced by blood pressure reduction. On the other hand, the influence of treatment on the atherosclerotic process or on the course of coronary artery disease and its complications is not currently understood. The accelerating effect of hypertension on atherosclerosis generally requires a critical level of circulating lipoproteins. Enhanced atherosclerosis is not observed in hypertensive animals without hyperlipoproteinemia or in human subjects with low lipoprotein concentrations.(ABSTRACT TRUNCATED AT 400 WORDS)
D000375:Aging; D000818:Animals; D001158:Arteries / Q000473:pathology / Q000503:physiopathology; D001161:Arteriosclerosis / Q000209:etiology; D001773:Blood Cells / Q000473:pathology; D002448:Cell Adhesion; D002463:Cell Membrane Permeability; D002561:Cerebrovascular Disorders / Q000209:etiology; D003094:Collagen / Q000378:metabolism; D003326:Coronary Circulation; D003900:Desoxycorticosterone; D004727:Endothelium / Q000166:cytology / Q000473:pathology / Q000503:physiopathology; D006973:Hypertension / Q000139:chemically induced / Q000150:complications / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D008854:Microscopy, Electron; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D012306:Risk; D012965:Sodium Chloride
D003900:Desoxycorticosterone; D012965:Sodium Chloride; D003094:Collagen