Abstract
Atherosclerosis results from multiple factors and involves several mechanisms, including endothelialmonocyte and smooth muscle cell (SMC) changes, cholesterol accumulation, plaque rupture andthromboembolism. Calcium ions play a role in the initial and chronic development of atheroscleroticlesions. Several studies in experimental animal models have demonstrated the potential direct antiatheroscleroticeffects of calcium antagonists. In this study the antiatherogenic activity of lercanidipine, anew lipophilic, second-generation calcium antagonist, was investigated. Lercanidipine and itsenantiomers inhibited the replication and migration of arterial myocytes in concentrations ranging from10 to 50 µM. The antiproliferative effect of lercanidipine was dose dependent, with a potency similar tothat of lacidipine and nifedipine, and was unrelated to the stereoselectivity of enantiomers to bind L-typecalcium channels. Lercanidipine and its enantiomers (25 µM) decreased the serum-induced elevation of[Ca2+]i in SMC, with the (S)-enantiomer (69% inhibition) being 2.4-fold more active than the (R)-counterpart (29% inhibition). The studies performed with enantiomers of lercanidipine suggest that theobserved effects are not related to the blockade of voltage-dependent Ca2+ channels and confirm, at leastin vitro, the pharmacological potential of the compound to influence negatively the process of atherogenesis.
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