The relationship of hypertension to coronary, aortic, and iliofemoral atherosclerosis.
Evidence from actuarial statistics, epidemiologic studies, and laboratory experiments clearly indicates that hypertension has an accelerating effect on atherogenesis, and this atherogenesis appears to be a graded function of elevated intra-arterial pressure. The fact that atherosclerosis occurs preferentially in the abdominal aorta and iliofemoral arteries seems likely to result from the pressure augmentation by reflected pulse waves that is intensified by vasoconstriction and also by the increase in hydrostatis pressure that results from gravitational stress during standing. Vasoconstriction is a characteristic of hypertension and occurs also with upright posture. The predilection of the coronary epicardial vessels for atherosclerosis seems likely to relate to subtle pressure-volume changes in these arteries as a result of this vascular bed being in the highest pressure area of the arterial system and because intramyocardial arterial branches are completely occluded during systole. The possibility is presented that hypertension accelerates atherosclerosis because it is a metabolic determinant of the multifunctional arterial smooth muscle cells which have the potential for forming collagen and mucopolysaccharides as well as phospholipid.
D000818:Animals; D001012:Aorta, Abdominal; D001018:Aortic Diseases / Q000209:etiology; D001161:Arteriosclerosis / Q000209:etiology* / Q000378:metabolism; D001794:Blood Pressure; D003094:Collagen / Q000096:biosynthesis; D003326:Coronary Circulation; D003327:Coronary Disease / Q000209:etiology; D004285:Dogs; D005263:Femoral Artery; D006112:Gravitation; D006801:Humans; D006874:Hydrostatic Pressure; D006973:Hypertension / Q000150:complications* / Q000378:metabolism; D007083:Iliac Artery; D009130:Muscle, Smooth / Q000378:metabolism; D010743:Phospholipids / Q000096:biosynthesis; D011187:Posture; D013610:Tachycardia / Q000150:complications
D010743:Phospholipids; D003094:Collagen