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Cardiovascular Research 2006 71(3):411-413; doi:10.1016/j.cardiores.2006.06.006
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Copyright © 2006, European Society of Cardiology

Translocation of endothelial nitric oxide synthase: Another feat of amlodipine, a cardiovascular jack-of-all-trades

Bernd Mayer

Department of Pharmacology and Toxicology, Karl-Franzens University Graz, Univ.-Platz 2, A-8010 Graz, Austria

Received 29 May 2006; accepted 2 June 2006

The first 10% of the full text of this article appears below.

See article by Batova et al. [12] (pages 478–485) in this issue.

The antihypertensive drug amlodipine (Norvasc®) is a long-acting, third-generation Ca2+ channel blocker that has been shown to limit the progression of atherosclerosis and to decrease the incidence of cardiovascular events in humans [1]. It is generally well tolerated and often used in combination with diuretics, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor antagonists and statins [2–4]. Amlodipine exhibits nanomolar affinity to dihydropyridine as well as benzothiazepine and phenylalkylamine binding sites of voltage-dependent L-type Ca2+ channels [5]. It is several-fold more lipophilic than the first- and second-generation Ca2+ channel blockers and adopts a well-defined position in the bilayer membrane [6]. It has been . . . [Full Text of this Article]


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