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Cardiovascular Research 2003 59(4):807-809; doi:10.1016/S0008-6363(03)00525-X
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Amlodipine and endothelial nitric oxide synthase activity

Reza Tabrizchi*

Division of Basic Medical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John’s, NL A1B 3V6, Canada

rtabrizc@mun.ca

* Tel.: +1-709-777-6864; fax: +1-709-777-7010.

Received 14 July 2003; revised 14 July 2003; accepted 16 July 2003

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

See article by Lenasi et al. [1] (pages 844–853) in this issue.

In an interesting and well crafted paper in this issue Lenasi et al. [1] have provided novel and exciting evidence on the ability of the 1,4-dihydropyridine Ca2+ channel antagonists, amlodipine and nifedipine, to generate nitric oxide (NO) and in doing so produce relaxation in the vasculature.

Admittedly, organic Ca2+ channel antagonists produce vasorelaxation predominantly by inhibiting the influx of Ca2+ into smooth muscle cells via the so-called voltage-gated Ca2+ channels [2]. However, there is empirical clinical data which implies that, in part, the cardiovascular protective actions of some Ca2+ channel antagonists cannot be readily explained purely on the basis of the inhibition of voltage-gated Ca2+ channels. For example, it has been reported that in the Prospective Randomized Amlodipine Survival Evaluation Study Group (PRAISE) trial, . . . [Full Text of this Article]


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