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      Antihypertensive Effects of Long-Acting Calcium Channel Blockers on Hemodialysis Days – A Randomized Crossover Trial between Benidipine and Nifedipine CR

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          Abstract

          Background/Aims: Since antihypertensive effects of most calcium channel blockers largely depend on their plasma concentrations, a rapid increase in blood pressure may occur as circulating levels of such blockers decrease after hemodialysis. Thus, the effects of benidipine and nifedipine CR (extended-release coated tablets, Adalat CR<sup>®</sup>), which are long-acting calcium channel blockers, on post-hemodialytic blood pressures were investigated. Methods: A randomized crossover trial was carried out with 10 hypertensive patients on chronic maintenance hemodialysis. Patients were assigned to receive benidipine (4–8 mg/day) or nifedipine CR (20–40 mg/day), and after 4 weeks, 24-hour ambulatory blood pressure monitoring was performed on the day of hemodialysis and blood samples were obtained before and after hemodialysis to measure plasma concentrations of the blockers. The calcium channel blockers were then exchanged in each patient and the same protocol was repeated. Results: The pattern of fluctuation of blood pressure differed markedly between the treatment with benidipine and nifedipine CR. Under treatment with nifedipine CR, rapid increase in blood pressure was observed after hemodialysis, while blood pressure remained at favorable levels with benidipine. Plasma concentrations of the blockers were significantly decreased by hemodialysis. Conclusion: Benidipine exerts more sustained antihypertensive effects than expected from its disposition in plasma. The stable depressor effects of benidipine even after hemodialysis may contribute to favorable control of blood pressure in this population.

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          Most cited references 3

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          Effect of long-acting and short-acting calcium antagonists on cardiovascular outcomes in hypertensive patients.

          Short-acting calcium antagonists may increase coronary artery morbidity, mortality, and non-cardiovascular complications in hypertensive patients. We assessed whether this association was also true for long-acting calcium antagonists.
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            ACE genotype and ACE inhibitor response in kidney disease: a perspective.

             Gert Mayer (2002)
            Angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce blood pressure and slow the progression of renal diseases. However, a substantial interindividual variability in treatment response also has been noted. The activity of ACE is partially dependent on the presence or absence of a 287-bp element in intron 16, and this insertion/deletion (I/D) polymorphism accounts for 47% of the total phenotypic variance in plasma ACE; DD subjects have the highest; ID subjects, intermediate; and II individuals, the lowest concentrations. Data suggest that genotype also determines tissue enzyme activity, and, at least under certain conditions, ACE activity is a rate-limiting step for angiotensin II formation. It therefore has been speculated that the ACE polymorphism also might affect therapeutic effects of ACE inhibitors. Unfortunately, clinical studies performed to date do not allow us to draw definite conclusions. Nonetheless, the rapidly evolving area of pharmacogenomics soon will also affect therapeutic decisions in the field of nephrology and hypertension. Copyright 2002 by the National Kidney Foundation, Inc.
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              Blunted Nocturnal Blood Pressure Decrease and Left-Ventricular Mass in Hypertensive Hemodialysis Patients

              Left-ventricular hypertrophy (LVH) represents a frequent complication in hemodialysis (HD) patients. Hypertension is a well-known risk factor of cardiac morbidity which is present in 2 of 3 patients: among them about 60% have a blunted nocturnal decrease of blood pressure (BP). Although some large studies on essential hypertensives have documented that non-dipper patients have a higher number of cardiac events and a higher left ventricle (LV) mass than dipper ones, conflicting results have been reported for dialysis patients. Therefore, the aim of our study was to assess differences in LV mass between dipper and non-dipper hypertensive HD patients. We studied 66 patients with 24-hour ambulatory BP monitoring performed on HD and on inter-HD day. They were classified as dipper when a decrease of at least 10% of nocturnal systolic blood pressure on the inter-HD day was present. Echocardiography and bioimpedance were performed. 29% of the patients were classified as dippers and 71% as non-dippers. The 48-hour systolic and diastolic BP were not significantly different between the two groups (SBP: dipper = 144 ± 12.9 mm Hg, non-dipper = 149 ± 17.8 mm Hg; DBP: dipper = 80 ± 9.9 mm Hg, non-dipper = 81 ± 10.6 mm Hg). LV mass index (LVMi) did not differ between the two groups (dipper = 143.1 ± 40.7 g/m 2 ; non-dipper = 159.4 ± 46.3 g/m 2 ). No differences were reported between dipper and non-dipper patients regarding extracellular water distribution (ECW: 48.1 ± 7.7 vs. 49.8 ± 10.8%). SBP night/day ratio and 48-hour SBP were not correlated to LVMi. A strong correlation was reported between ECW% and LVMi (r = 0.53, p < 0.001). In conclusion, 2 of 3 hypertensive HD patients are non-dipper, and this condition does not seem to be associated with significant differences in 48-hour blood pressure and LV mass. Volume overload appears to be the main independent determinant of LVH in these patients.
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                Author and article information

                Journal
                NEC
                Nephron Clin Pract
                10.1159/issn.1660-2110
                Nephron Clinical Practice
                S. Karger AG
                1660-2110
                2004
                June 2004
                17 November 2004
                : 97
                : 2
                : c49-c53
                Affiliations
                aDepartment of Internal Medicine, Komono Kosei Hospital, Komono, bDepartment of Internal Medicine, Johoku Hospital, Nagoya, and cInternal Medicine and Molecular Science, Nagoya City University Graduate School, Nagoya, Japan
                Article
                78400 Nephron Clin Pract 2004;97:c49–c53
                10.1159/000078400
                15218330
                © 2004 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 1, Tables: 2, References: 20, Pages: 1
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/78400
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