Effect of the new calcium antagonist lercanidipine and its enantiomers on the migration and proliferation of arterial myocytes

Journal of Cardiovascular Pharmacology
A CorsiniR Fumagalli

Abstract

The in vitro effects were investigated of the new dihydropyridine calcium antagonist (CA) lercanidipine and its enantiomers on arterial myocyte (smooth muscle cell; SMC) migration and proliferation as related to L-type calcium channel inhibition. Lercanidipine and its enantiomers inhibited the replication and migration of arterial myocytes in concentration ranging from 10 to 50 microM. The antiproliferative effect of lercanidipine, evaluated as cell number, 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. The cell doubling time increased with drug concentration < or = 122 versus 38 h for controls. The cell growth inhibition induced by lercanidipine and its enantiomers was reversible. Lercanidipine dose dependently decreased [3H]thymidine incorporation into DNA; the (R)-enantiomer, displaying the lowest CA activity, was the most potent in this respect. The tested compounds were able to inhibit fibrinogen-induced myocyte migration in a dose-dependent manner, with the (R)-enantiomer showing the more pronounced effect. To directly rule out the role of calcium channels in the antiatherosclerotic properties of le...Continue Reading

References

Sep 1, 1978·The American Journal of Physiology·K M BaldwinR E Lewis
Dec 1, 1975·Journal of Cellular Physiology·E Elmore, M Swift
Nov 1, 1992·Circulation·D Waters, J Y Lam
Dec 1, 1992·Hypertension·C L Jackson, S M Schwartz
Jan 1, 1990·Journal of Cardiovascular Pharmacology·P D Henry
Jan 1, 1991·Journal of Cardiovascular Pharmacology·W G Nayler, S Britnell
Jun 1, 1990·Proceedings of the National Academy of Sciences of the United States of America·D GordonS M Schwartz
Jun 1, 1990·Journal of the American College of Cardiology·J H IpJ H Chesebro
Jan 1, 1990·Annals of the New York Academy of Sciences·R W WisslerA Komatsu
Nov 7, 1989·The American Journal of Cardiology·F BerniniR Paolétti
Nov 1, 1989·Atherosclerosis·C L JacksonD E Bowyer
Apr 29, 1988·Biochemical and Biophysical Research Communications·D RampeA M Brown
Apr 1, 1986·Circulation Research·S M SchwartzJ H Campbell
Nov 1, 1993·The American Journal of Physiology·Z WangL J Mordan
May 1, 1993·Pharmacological Research : the Official Journal of the Italian Pharmacological Society·A CorsiniR Paoletti
Mar 1, 1993·Journal of Hypertension. Supplement : Official Journal of the International Society of Hypertension·F BerniniR Paoletti
Feb 1, 1996·Journal of Cardiovascular Pharmacology·F GrazianiF T van Amsterdam

❮ Previous
Next ❯

Citations

Dec 21, 2000·Current Atherosclerosis Reports·S Bellosta, F Bernini
Mar 6, 1998·International Journal of Cardiology·M Schachter
May 26, 2012·Toxicology and Applied Pharmacology·Joshua K SalabeiDaniel J Conklin
Aug 28, 2007·Experimental Physiology·Yeshavanth K Banasavadi SiddegowdaSantosh K Mishra
Mar 31, 2015·Journal of Analytical Methods in Chemistry·Luciana Pereira LourençoCristiane Masetto de Gaitani
Jul 20, 2014·Journal of the Renin-angiotensin-aldosterone System : JRAAS·Adrian DrapalaMarcin Ufnal
Jun 2, 2012·Journal of Atherosclerosis and Thrombosis·Norio IshiiEiichi Araki
Sep 27, 2003·Arteriosclerosis, Thrombosis, and Vascular Biology·R P MasonT H Hintze
Nov 8, 2005·American Journal of Physiology. Heart and Circulatory Physiology·Utako YokoyamaYoshihiro Ishikawa
Sep 25, 2004·American Journal of Physiology. Heart and Circulatory Physiology·Mark B KahnThomas N Tulenko
Jan 16, 2002·Journal of Hypertension·Olivier StepienPierre Marche
Dec 6, 2000·Immunopharmacology and Immunotoxicology·R L SciorsciP Minoia
Sep 20, 2000·American Journal of Physiology. Heart and Circulatory Physiology·O Stepien, P Marche
Jul 30, 2014·Journal of the Renin-angiotensin-aldosterone System : JRAAS·Nicola FerriAlberto Corsini
May 1, 2021·International Journal of Molecular Sciences·Maria Giovanna LupoNicola Ferri

❮ Previous
Next ❯

Related Concepts

Related Feeds

Atherosclerosis Disease Progression

Atherosclerosis is the buildup of plaque on artery walls, causing stenosis which can eventually lead to clinically apparent cardiovascular disease. Find the latest research on atherosclerosis disease progression here.