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      Effect of L-Dopa Decarboxylase Inhibitor Benserazide on Renal Function in Streptozotocin-Diabetic Rats

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          Abstract

          Background/Aims: Benserazide (BZD), an inhibitor of the dopamine synthesis, abolished the increase in glomerular filtration rate (GFR) following the infusion of a mixed amino acid solution. These results reveal endogenous dopamine as a mediator in the renal response to amino acids. The aim of the present study was to evaluate whether dopamine is also involved in the regulation of glomerular hyperfiltration during the early state of diabetes mellitus (DM). Methods: Male Sprague-Dawley rats were injected with a single dose of streptozotocin (60 mg/kg i.p.) for induction of experimental DM (n = 7–8/group). Age-matched non-diabetic animals, injected with citrate buffer, served as controls (CON, n = 8/group). Clearance experiments were performed 2 weeks after induction of DM in thiopental-anesthetized rats (80 mg/kg i.p.), which were continuously infused either with BZD (30 µg/min/kg) or vehicle (VHC). Results: Mean arterial blood pressure was around 110 mm Hg and did not significantly differ among the groups. GFR was 0.95 ± 0.02 ml/min/100 g b.w. in VHC-treated CON. BZD treatment did not significantly change GFR in the CON group (0.92 ± 0.06 ml/min/100 g b.w.). As expected, glomerular hyperfiltration was observed in diabetic rats infused with VHC (1.24 ± 0.08 ml/min/100 g b.w.). Treatment with BZD significantly reduced the diabetes-induced increase in GFR to control levels (0.95 ± 0.05 ml/min/100 g b.w.). Conclusion: Our results show that the inhibition of dopamine synthesis prevented the increase in GFR due to diabetic conditions, indicating that endogenous dopamine is involved in the regulation of DM-induced changes in renal hemodynamics.

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          Most cited references 11

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          Renal functional reserve in humans

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            Early glomerular hyperfiltration in insulin-dependent diabetics and late nephropathy.

             C E Mogensen (1986)
            The aim of this study was to clarify whether early glomerular hyperfiltration, a characteristic feature of insulin-dependent diabetes, is associated with late diabetic nephropathy. In 1984 we re-examined 12 patients previously investigated in our laboratory around 1970; entrance criteria were as follows: male diabetics, clearly insulin-dependent, and age at onset of diabetes less than or equal to 20 years; glomerular filtration rate (GFR) and renal plasma flow (RPF) measured at least 7 years before follow-up study; duration of diabetes at initial examination 3-7 years. All patients fulfilling these criteria accepted a re-examination. The end-point at follow-up (final criterium) was the level of urinary albumin excretion (UAE), either elevated (greater than or equal to 15 micrograms/min) or normal (less than 15 micrograms/min). A clear discrimination was seen, patients being either grossly abnormal (95-4117 micrograms/min) or normal (2.6-7.4 micrograms/min). A marked difference in initial GFR was seen: 166 ml/min +/- 15.4 in those with high UAE at follow-up versus 138 +/- 8.6 in patients with normal UAE at follow-up (2p = 0.2%). The GFR at follow-up was significantly decreased in diabetics with high follow-up UAE (mean values 166----80 ml/min) but stable in patients with low UAE (138----132 ml/min). Initial blood pressure, plasma glucose and RPF were not different between groups. Marked glomerular hyperfiltration, whatever its cause, may contribute to late glomerular damage in diabetic nephropathy. Early measurements of GFR and UAE can be used to identify patients at risk of subsequently developing nephropathy.
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              Chronic renal denervation prevents glomerular hyperfiltration in diabetic rats.

              The increase in glomerular filtration rate (GFR) induced by amino acid infusion is attenuated in rats with chronic renal denervation. The aim of the present study was to investigate whether renal denervation abrogates glomerular hyperfiltration occurring in the early state of diabetes mellitus. Sprague-Dawley rats were subjected to bilateral renal denervation before induction of diabetes mellitus (DM) by streptozotocin. Clearance experiments were performed 2 weeks after onset of moderate DM. Glomerular volume was estimated following paraformaldehyde fixation in rat kidney slices from measurement of cross-sectional area of Bowman's capsule. GFR in non-diabetic rats with intact nerves (CON-INN) was 0.82+/-0.03 ml.min(-1).100 g(-1) body weight. Diabetic animals with innervated kidneys presented a significant glomerular hyperfiltration (1.13+/-0.03 ml.min(-1).100 g(-1) body weight), while renal denervation in diabetic rats lowered GFR towards levels of CON-INN (0.88+/-0.03 ml.min(-1).100 g(-1) body weight). Estimated glomerular volume amounted to 0.69+/-0.03.10(6) micro m(3) in the CON-INN group and was significantly higher in diabetic animals with intact renal nerves (0.86+/-0.04.10(6) microm(3)). Interestingly, renal denervation prevented the glomerular enlargement due to DM. Renal nerves appear to be significantly involved in the mediation of glomerular hyperfiltration in experimental DM. If the kidney is prevented from sympathetic nerve stimulation, structural changes due to early diabetic nephropathy, i.e. glomerular enlargement, are abolished.
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                Author and article information

                Journal
                KBR
                Kidney Blood Press Res
                10.1159/issn.1420-4096
                Kidney and Blood Pressure Research
                S. Karger AG
                1420-4096
                1423-0143
                2006
                June 2006
                06 June 2006
                : 29
                : 1
                : 43-47
                Affiliations
                Department of Pharmacology and Toxicology, Faculty of Medicine, University of Tübingen, Tübingen, Germany
                Article
                92849 Kidney Blood Press Res 2006;29:43–47
                10.1159/000092849
                16636577
                © 2006 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: 2, Tables: 1, References: 17, Pages: 5
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/92849
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