This Article Full Text Full Text (PDF) All Versions of this Article: 42/4/e10    most recent 01.HYP.0000091372.14174.89v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Tomlinson, B. Articles by Salvetti, A. Search for Related Content PubMed PubMed Citation Articles by Tomlinson, B. Articles by Salvetti, A. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information Antioxidants Related Collections Cardiovascular Pharmacology Clinical Studies Endothelium/vascular type/nitric oxide

(Hypertension. 2003;42:e10.)
© 2003 American Heart Association, Inc.

Letters to the Editor

Antioxidant Effect of Lercanidipine

Department of Medicine and Therapeutics, The Chinese University of Hong Kong

Iris F.F. Benzie

Ageing and Health Section, School of Nursing, The Hong Kong Polytechnic University

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We were surprised by the effects of lercanidipine reported by Taddei et al¹ on the plasma antioxidant capacity, with the ferric reducing (antioxidant) power (FRAP) value increasing from 305.0±31.3 to 435.7±142.9 µmol/L. Typical FRAP values for human plasma usually range from 800 to 1200 µmol/L.² The apparently low baseline values may be related to the use of ascorbic acid or Trolox^TM (rather than a solution of ferrous ions) as calibrator without correcting for their stoichiometric factor, which is 2.0 in the FRAP assay. However, it is more difficult to explain the almost 50% increase in plasma FRAP values after lercanidipine treatment. We have found that lercanidipine itself has no in vitro antioxidant effect in the FRAP assay, but it does undergo extensive first-pass metabolism, and some metabolites could have a direct antioxidant effect. The peak plasma concentration (C_max) of S-lercanidipine is, at most, around 15 nmol/L,^3,4 and although the C_max for total metabolites was >40 times higher than that of the parent drug,⁵ this still amounts to <1 µmol/L of total metabolites. Even if each molecule of metabolite could scavenge several radicals, it is highly unlikely that this would have any appreciable direct effect on the plasma FRAP value. Similarly, captopril has virtually no contribution to plasma FRAP in vivo, despite having in vitro antioxidant activity.⁶

In contrast, plasma ascorbic acid at normal plasma concentrations (40 to 60 µmol/L) contributes about 15% of the total FRAP value. Bilirubin and -tocopherol each contribute about 5%, plasma proteins . . . [Full Text of this Article]

Stefano Taddei; Agostino Virdis; Lorenzo Ghiadoni; Daniele Versari; Guido Salvetti; Armando Magagna; Antonio Salvetti

Department of Internal Medicine, University of Pisa, Pisa, Italy