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      Role of Thyroid Hormones on the Synthesis and Release of Atrial Natriuretic Peptide in Rats with Acute Renal Failure

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          Abstract

          Background/Aims: High atrial natriuretic peptide (ANP) serum levels are seen in acute renal failure (ARF) due to impaired ANP clearance, but the response of ANP to blood volume expansion is blunted. ARF-associated hypothyroidism influences ANP clearance but it may also play a role in the synthesis and release of ANP because in primary hypothyroidism both mechanisms are disturbed. The aim of this study is to analyze whether thyroxin (T<sub>4</sub>) supplementation improves the synthesis and release of ANP in ARF. Methods: Four groups of rats were studied: group C (control); group ARF; Group ARF-T<sub>4</sub> (ARF supplemented with T<sub>4</sub>), and group Tx (thyroidectomized). Serum creatinine (SCr), creatinine clearance (CrCl), total T<sub>4</sub>, total triiodothyronin (T<sub>3</sub>), plasma ANP, ANP response to acute saline load and atrial content of mRNA-ANP were measured 5 days after ARF induction with potassium dichromate. Results: CrCl was 1.8 ± 0.4 ml/min in group C, and it significantly dropped to 0.6 ± 0.5 in ARF (p < 0.01), T<sub>4</sub> improved it (1.7 ± 0.7 in ARF-T<sub>4</sub>, p < 0.01) and Tx did not change it. Plasma ANP was higher in ARF as compared with C (152 ± 23 vs. 52 ± 21 fmol/l, p < 0.01). In ARF-T<sub>4</sub>, ANP was higher than in C but lower than in ARF (85 ± 28 fmol/l, p < 0.01). No changes were observed in Tx rats (48 ± 17 fmol/l). The atrial content of mRNA-ANP was 0.06 ± 0.025 mRNA-ANP/mRNA-β-actin ratio units in group C, it was higher in ARF (0.13 ± 0.025, p < 0.01) and lower in Tx (0.04 ± 0.01, p < 0.05) as compared to C. Supplementation with T<sub>4</sub> increased the mRNA-ANF content (0.18 ± 0.2 mRNA-ANP/mRNA-β-actin ratio units, p < 0.05) over ARF. Plasma ANP response to saline load was 45 ± 7% in C, but it was reduced in ARF and Tx (20 ± 10 and 26 ± 10%, p < 0.01). In ARF-T<sub>4</sub> the response was restored (36 ± 9%, p < 0.01 vs. ARF). Conclusion: Thyroid hormones modulate the synthesis and release of ANP in ARF. Although the effect is probably direct, T<sub>4</sub>-induced amelioration of renal damage may also play a significant role by improving the uremic milieu.

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          Most cited references 3

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          Sodium iodide symporter in health and disease.

          Radioiodine-concentrating activity in thyroid tissues has allowed the use of radioiodine as a diagnostic and therapeutic agent for patients with thyroid disorders such as well-differentiated thyroid cancer. However, some extrathyroidal tissues also take up radioiodine, contributing to unwanted side effects of radioiodine therapy. Now that the molecule that mediates radioiodine uptake, the sodium iodide symporter (NIS), has been cloned and characterized, it may be possible to develop novel strategies to differentially modulate NIS expression and/or activity, enhancing it in target tissues and impeding it in others. In addition to restoring NIS expression/activity to ensure sufficient radioiodine uptake for the diagnosis and treatment of advanced thyroid cancers, we envision that it may be possible to selectively increase or confer NIS expression/activity in tumors of nonthyroidal tissues to facilitate the use of radioiodine in their diagnosis and treatment. We also consider the molecular basis of thyroid and nonthyroid disorders that may be complicated by NIS deregulation. Finally, we explore the use of NIS as an imaging reporter gene to monitor the expression profile of the transgene in transgenic mouse animal models and in patients undergoing gene therapy clinical trials.
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            Epidemiology of De Novo Acute Renal Failure in Hospitalized African Americans

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              Altered thyroidal status and the in vivo synthesis of atrial natriuretic peptide in the rat heart.

              The effect of altered thyroidal status on levels of immunoreactive (ir)- atrial natriuretic peptide (ANP) in serum and the four cardiac chambers, and of tissue ANP mRNA, was determined in groups of rats given vehicle, thyroxine (T4), propylthiouracil (PTU) or T4 plus PTU for 3 weeks. Serum levels of ir-ANP were approximately 3-fold higher in T4-treated animals compared with control; levels in PTU or PTU/T4 groups were not different from control. Right ventricular ANP mRNA was below detection; in other chamber, levels rose with T4, alone or plus PTU, and fell after PTU compared with control. Atrial ir-ANP levels were unchanged by T4, but increased (left atrium, LA) or decreased (right atrium, RA) after PTU alone. After PTU/T4, some indices (e.g. tissue weight) remained at control levels, others (e.g. ANP mRNA levels) were equivalent to levels in the T4-alone group, and others (e.g. LA ir-ANP) were equivalent to those seen with PTU alone. We conclude that the role of thyroid hormones on ANP synthesis may be similar between chambers but their effects on release appear to differ widely. The extent to which this represents secondary rather than direct effects, or possible T3-versus T4-specific events, awaits elucidation.
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                Author and article information

                Journal
                NEE
                Nephron Exp Nephrol
                10.1159/issn.1660-2129
                Cardiorenal Medicine
                S. Karger AG
                1660-2129
                2003
                September 2003
                17 November 2004
                : 95
                : 1
                : e24-e29
                Affiliations
                Unidad de Investigación Médica en Enfermedades Nefrológicas, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, México, México
                Article
                73020 Nephron Exp Nephrol 2003;95:e24–e29
                10.1159/000073020
                14520011
                © 2003 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: 3, Tables: 1, References: 29, Pages: 1
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/73020
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