抄録
Current evidences suggest that calcium may play a pathogenic role in atherosclerosis. In cholesterolfed rabbits, calcium channel blockers such as nifedipine, verapamil and diltiazem have been demonstrated to exert antiatherogenic effects without reducing the diet-induced hypercholesterolemia. In the present study, rat aortic smooth muscle cells (SMC) were used to study the effects of verapamil, diltiazem and nicorandil on cellular interactions with human low density lipoprotein (LDL). Specific bindings of 125I-LDL to SMC were not significantly changed by these drugs. Specific internalization were significantly increased by verapamil and diltiazem at concentration of 10-4M compared to control. Only verapamil of three agents decreased significantly specific degradation of 125I-LDL at concentration of 10-4M. Nicorandil, 10-8 to 10-4M, did not affect catabolism of 125I-LDL in SMC. These findings indicated that these drugs affect the intracellular catabolism of LDL differently in SMC.
