Parmley W W
Division of Cardiology, University of California School of Medicine, San Francisco 94143.
Am J Cardiol. 1990 Dec 18;66(21):16I-22I. doi: 10.1016/0002-9149(90)91259-9.
Atherosclerosis is the result of complex, interrelated processes, many of which involve calcium. Interventions that interfere with calcium uptake by cells retard lesion development in experimental models of atherosclerosis, underscoring calcium's critical role in atherogenesis. A wide variety of calcium antagonists, including nifedipine, verapamil and diltiazem, have been shown to protect against atherosclerosis in animal models. While these drugs are quite different from each other pharmacologically, they all block intracellular calcium influx. This common property is thus the proposed mechanism for their antiatherosclerotic effects. The effectiveness of the calcium antagonists against the development of atherosclerosis in experimental models may be relevant in the selection of antihypertensive therapy--provided that their protective effects can be demonstrated in future clinical trials as well.
动脉粥样硬化是复杂且相互关联的过程的结果，其中许多过程都涉及钙。在动脉粥样硬化实验模型中，干扰细胞摄取钙的干预措施会延缓病变发展，这突出了钙在动脉粥样硬化形成中的关键作用。多种钙拮抗剂，包括硝苯地平、维拉帕米和地尔硫䓬，已在动物模型中显示出对动脉粥样硬化有预防作用。虽然这些药物在药理学上彼此差异很大，但它们都能阻断细胞内钙内流。因此，这一共同特性被认为是它们抗动脉粥样硬化作用的机制。钙拮抗剂在实验模型中对动脉粥样硬化发展的有效性可能与抗高血压治疗的选择相关——前提是它们的保护作用也能在未来的临床试验中得到证实。
