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      Renal Dopaminergic System Activity in Uninephrectomized Rats up to 26 Weeks after Surgery

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          Abstract

          Background: Dopamine of renal origin exerts natriuretic and diuretic effects by activating D<sub>1</sub>-like receptors located at various regions in the nephron. Two weeks after uninephrectomy the renal dopaminergic system was suggested to be involved in the adaptative increase of sodium excretion. Aim: The aim of the present study was to evaluate the renal adaptations in sodium handling and renal dopaminergic system activity in uninephrectomized (Unx) rats up to 26 weeks after the surgery. Results: A time-dependent increase in both systolic and diastolic blood pressure was observed in Unx rats up to 26 weeks after uninephrectomy. This was accompanied by a compensatory increase in aromatic L-amino acid decarboxylase at 2 weeks but not 10 and 26 weeks after uninephrectomy. In contrast to what has been found 2 weeks after uninephrectomy, at 10 and 26 weeks after surgery the natriuretic response to volume expansion was reduced in Unx rats and this was accompanied by insensitivity of natriuresis to dopamine D1 receptor selective antagonist (Sch23390). Conclusion: A time-dependent decrease in dopamine sensitive natriuresis is observed in Unx rats throughout the 26 weeks after uninephectomy. It is suggested that this may contribute to compromise sodium excretion and increase blood pressure.

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          Most cited references 11

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          Living-donor kidney transplantation: a review of the current practices for the live donor.

          The first successful living-donor kidney transplant was performed 50 yr ago. Since then, in a relatively brief period of medical history, living kidney transplantation has become the preferred treatment for those with ESRD. Organ replacement from either a live or a deceased donor is preferable to dialysis therapy because transplantation provides a better quality of life and improved survival. The advantages of live versus deceased donor transplantation now are readily apparent as it affords earlier transplantation and the best long-term survival. Live kidney donation has also been fostered by the technical advance of laparoscopic nephrectomy and immunologic maneuvers that can overcome biologic obstacles such as HLA disparity and ABO or cross-match incompatibility. Congressional legislation has provided an important model to remove financial disincentives to being a live donor. Federal employees now are afforded paid leave and coverage for travel expenses. Candidates for renal transplantation are aware of these developments, and they have become less hesitant to ask family members, spouses, or friends to become live kidney donors. Living donation as practiced for the past 50 yr has been safe with minimal immediate and long-term risk for the donor. However, the future experience may not be the same as our society is becoming increasingly obese and developing associated health problems. In this environment, predicting medical futures is less precise than in the past. Even so, isolated abnormalities such as obesity and in some instances hypertension are no longer considered absolute contraindications to donation. These and other medical risks bring additional responsibility in such circumstances to track the unknown consequences of a live-donor nephrectomy.
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            Intrarenal dopamine: a key signal in the interactive regulation of sodium metabolism.

             A Aperia (1999)
            The kidney regulates sodium metabolism with extraordinary precision and sensitivity. This is accomplished by an intricate interaction between signals from extrarenal and intrarenal sources and between anti-natriuretic and natriuretic factors. Dopamine, produced in renal proximal tubule cells, plays a central role in this interactive network. Natriuretic hormones that are released from extrarenal sources, such as atrial natriuretic peptide, mediate some of their effects via renal dopamine receptors. On the level of the tubules, dopamine acts by opposing the effects of anti-natriuretic factors, such as angiotensin II and alpha-adrenergic receptors. Sodium retention leads to an increase in renal dopamine tonus, and the natriuretic effects of dopamine are more prominent under this condition. Inhibition or down-regulation of dopamine receptors significantly attenuates the natriuretic response to salt loading. Renal dopamine is modulated by the supply of filtered L-DOPA and the metabolism of dopamine via catechol-O-methyldopamine. The importance of dopamine as a natriuretic hormone is reflected by its capacity to inhibit the majority of renal tubule sodium transporters. Notably, the activity of Na+, K+ ATPase is inhibited in most tubule segments by dopamine. Recent studies have elucidated many of the signaling pathways for renal dopamine receptors. Novel principles for homologous and heterologous sensitization of dopamine receptors have been detected that may explain some of the interaction between dopamine and other first messengers that modulate renal tubule sodium transport. A broad understanding of the renal dopamine system has become increasingly important, since there is now strong evidence from both clinical and experimental studies that dysregulation of the renal dopamine system plays a role in many forms of multigenetic hypertension.
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              Renal dopamine receptors in health and hypertension.

              During the past decade, it has become evident that dopamine plays an important role in the regulation of renal function and blood pressure. Dopamine exerts its actions via a class of cell-surface receptors coupled to G-proteins that belong to the rhodopsin family. Dopamine receptors have been classified into two families based on pharmacologic and molecular cloning studies. In mammals, two D1-like receptors that have been cloned, the D1 and D5 receptors (known as D1A and D1B, respectively, in rodents), are linked to stimulation of adenylyl cyclase. Three D2-like receptors that have been cloned (D2, D3, and D4) are linked to inhibition of adenylyl cyclase and Ca2+ channels and stimulation of K+ channels. All the mammalian dopamine receptors, initially cloned from the brain, have been found to be expressed outside the central nervous system, in such sites as the adrenal gland, blood vessels, carotid body, intestines, heart, parathyroid gland, and the kidney and urinary tract. Dopamine receptor subtypes are differentially expressed along the nephron, where they regulate renal hemodynamics and electrolyte and water transport, as well as renin secretion. The ability of renal proximal tubules to produce dopamine and the presence of receptors in these tubules suggest that dopamine can act in an autocrine or paracrine fashion; this action becomes most evident during extracellular fluid volume expansion. This renal autocrine/paracrine function is lost in essential hypertension and in some animal models of genetic hypertension; disruption of the D1 or D3 receptor produces hypertension in mice. In humans with essential hypertension, renal dopamine production in response to sodium loading is often impaired and may contribute to the hypertension. The molecular basis for the dopaminergic dysfunction in hypertension is not known, but may involve an abnormal post-translational modification of the dopamine receptor.
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                Author and article information

                Journal
                AJN
                Am J Nephrol
                10.1159/issn.0250-8095
                American Journal of Nephrology
                S. Karger AG
                0250-8095
                1421-9670
                2007
                May 2007
                27 March 2007
                : 27
                : 3
                : 232-239
                Affiliations
                aUnit of Research and Development of Nephrology, and bInstitute of Pharmacology and Therapeutics, Faculty of Medicine, Porto, Portugal
                Article
                101368 Am J Nephrol 2007;27:232–239
                10.1159/000101368
                17389783
                © 2007 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: 4, Tables: 3, References: 30, Pages: 8
                Categories
                Original Report: Patient-Oriented, Translational Research

                Cardiovascular Medicine, Nephrology

                Blood pressure, Renal mass reduction, Dopamine, Kidney

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