Atherogenesis and hypertension.
Low-density lipoprotein (LDL) is essential for the regulation of cellular cholesterol homeostasis. Intracellular LDL cholesterol metabolism is achieved by the action of lysosomal enzymes. The hydrolytic cleavage of cholesterol is apparently suppressed in the smooth muscle of arterial vessels of hypertensive animal models, contributing to atherosclerosis. The change in the hydrolytic activity of the enzymes can be reversed by Ca2+ antagonists which also lower increased blood pressure. Thus, a blood pressure lowering effect of calcium antagonists may explain the antiatherosclerotic action of these agents. Preliminary data, using platelets as a model for studies on LDL action, suggest that LDL induces rapid cellular activation via phosphatidylinositol turnover.
Department of Internal Medicine, Kantonsspital, Basel, Switzerland.
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D000118:Acetylglucosaminidase / Q000378:metabolism; D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology*; D001792:Blood Platelets / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications; D006973:Hypertension / Q000150:complications*; D008077:Lipoproteins, LDL / Q000097:blood; D009131:Muscle, Smooth, Vascular / Q000201:enzymology; D051381:Rats; D011918:Rats, Inbred SHR; D012307:Risk Factors; D002787:Sterol Esterase / Q000378:metabolism
D002121:Calcium Channel Blockers; D008077:Lipoproteins, LDL; D002787:Sterol Esterase; D000135:Acid Phosphatase; D000118:Acetylglucosaminidase