The new calcium antagonist lercanidipine and its enantiomers affect major processes of atherogenesis in vitro: Is calcium entry involved?

A. Corsini, M. R. Accomazzo, M. Canavesi, A. Sartani, R. Testa, A. L. Catapano, R. Fumagalli, R. Paoletti, F. Bernini

Research output: Contribution to journalArticle

Abstract

Atherosclerosis results from multiple factors and involves several mechanisms, including endothelial monocyte and smooth muscle cell (SMC) changes, cholesterol accumulation, plaque rupture and thromboembolism. Calcium ions play a role in the initial and chronic development of atherosclerotic lesions. Several studies in experimental animal models have demonstrated the potential direct antiatherosclerotic effects of calcium antagonists. In this study the antiatherogenic activity of lercanidipine, a new lipophilic, second-generation calcium antagonist, was investigated. Lercanidipine and its enantiomers inhibited the replication and migration of arterial myocytes in concentrations ranging from 10 to 50 μM. The antiproliferative effect of lercanidipine was dose dependent, with a potency similar to that of lacidipine and nifedipine, and was unrelated to the stereoselectivity of enantiomers to bind L-type calcium 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 the observed effects are not related to the blockade of voltage-dependent Ca2+ channels and confirm, at least in vitro, the pharmacological potential of the compound to influence negatively the process of atherogenesis.

Original languageEnglish
Pages (from-to)18-22
Number of pages5
JournalBlood Pressure, Supplement
Volume7
Issue number2
Publication statusPublished - 1998

Fingerprint

Atherosclerosis
Calcium
Smooth Muscle Myocytes
L-Type Calcium Channels
Thromboembolism
Nifedipine
Muscle Cells
Rupture
Monocytes
Animal Models
Cholesterol
lercanidipine
In Vitro Techniques
Pharmacology
Ions
Serum

Keywords

  • Atherosclerosis
  • Calcium antagonists
  • Cytosolic calcium
  • Fluo 3
  • L-type channels
  • Lercanidipine
  • Smooth muscle cells

ASJC Scopus subject areas

  • Internal Medicine
  • Cardiology and Cardiovascular Medicine

Cite this

The new calcium antagonist lercanidipine and its enantiomers affect major processes of atherogenesis in vitro : Is calcium entry involved? / Corsini, A.; Accomazzo, M. R.; Canavesi, M.; Sartani, A.; Testa, R.; Catapano, A. L.; Fumagalli, R.; Paoletti, R.; Bernini, F.

In: Blood Pressure, Supplement, Vol. 7, No. 2, 1998, p. 18-22.

Research output: Contribution to journalArticle

Corsini, A, Accomazzo, MR, Canavesi, M, Sartani, A, Testa, R, Catapano, AL, Fumagalli, R, Paoletti, R & Bernini, F 1998, 'The new calcium antagonist lercanidipine and its enantiomers affect major processes of atherogenesis in vitro: Is calcium entry involved?', Blood Pressure, Supplement, vol. 7, no. 2, pp. 18-22.
Corsini, A. ; Accomazzo, M. R. ; Canavesi, M. ; Sartani, A. ; Testa, R. ; Catapano, A. L. ; Fumagalli, R. ; Paoletti, R. ; Bernini, F. / The new calcium antagonist lercanidipine and its enantiomers affect major processes of atherogenesis in vitro : Is calcium entry involved?. In: Blood Pressure, Supplement. 1998 ; Vol. 7, No. 2. pp. 18-22.
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