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      Effects of Renal Perfusion Pressure on Renal Interstitial Hydrostatic Pressure and Na + Excretion: Role of Endothelium-Derived Nitric Oxide

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          Abstract

          The purpose of this study was to examine the role of endothelium-derived nitric oxide in modulating the effect of renal perfusion pressure (RPP) on renal interstitial hydrostatic pressure (RIHP) and urinary Na<sup>+</sup> excretion (UNaV). The effects of RPP on renal hemodynamics, RIHP, and Na<sup>+</sup> and Li<sup>+</sup> excretions were determined in control Sprague-Dawley rats, in Sprague-Dawley rats pretreated with intravenous infusion of N<sup>G</sup>-nitro- L-arginine methyl ester ( L-NAME) at doses of 1, 5, and 50 µg/kg/min, and in rats pretreated with L-NAME (5 µg/kg/min) plus L-arginine (10 mg/kg/min). The RPP was changed from 95 to 135 mm Hg by an electronically servo-controlled aortic occluder above the renal arteries in all groups. Increasing RPP in control rats from 95 to 135 mm Hg increased RIHP (from 4.4 ± 0.5 to 8.7 ± 1.2 mm Hg), UNaV (from 2.37 ± 0.61 to 8.29 ± 1.59 µEq/min), and fractional excretion of Li<sup>+</sup> (from 38.0 ± 2.5 to 51.4 ± 6.0%). In rats pretreated with L-NAME (5 µg/kg/min), increases in RPP from 95 to 135 mm Hg had no effect on RIHP (from 1.6 ± 0.4 to 2.2 ± 0.6 mm Hg) or fractional excretion of Li<sup>+</sup> and markedly attenuated pressure-natriuresis relationship (from 1.84 ± 0.50 to 2.88 ± 0.65 µEq/min). Although L-NAME did reduce renal plasma flow and glomerular filtration rate, the autoregulatory responses to RPP were maintained. In rats pretreated with L-NAME plus L-arginine, RIHP, UNaV, and fractional excretion of Li<sup>+</sup> responses to RPP were similar to the control rats. The results of this study indicate that endothelium-derived nitric oxide plays an important role in modulating the effect of RPP on Na<sup>+</sup> excretion by enhancing the transmission of RPP into the renal interstitium.

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          Most cited references 3

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          Vascular endothelial cells synthesize nitric oxide from L-arginine.

          Nitric oxide (NO) released by vascular endothelial cells accounts for the relaxation of strips of vascular tissue and for the inhibition of platelet aggregation and platelet adhesion attributed to endothelium-derived relaxing factor. We now demonstrate that NO can be synthesized from L-arginine by porcine aortic endothelial cells in culture. Nitric oxide was detected by bioassay, chemiluminescence or by mass spectrometry. Release of NO from the endothelial cells induced by bradykinin and the calcium ionophore A23187 was reversibly enhanced by infusions of L-arginine and L-citrulline, but not D-arginine or other close structural analogues. Mass spectrometry studies using 15N-labelled L-arginine indicated that this enhancement was due to the formation of NO from the terminal guanidino nitrogen atom(s) of L-arginine. The strict substrate specificity of this reaction suggests that L-arginine is the precursor for NO synthesis in vascular endothelial cells.
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            Arterial pressure regulation

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              Arginine is a physiological precursor of endothelium-derived nitric oxide.

              ATP dose dependently stimulated the formation and release of nitric oxide (NO) from perfused rabbit aorta. L-Canavanine, an inhibitor of various L-arginine-utilizing enzymes, abolished basal and ATP-induced NO formation and release. ATP increased the accumulation of presumably NO-derived NO2- in the medium of primary cultures of bovine aortic endothelial cells. 15NO, 15NO2- and 15NO3- formation was found when L-[guanido-15N2]arginine was added to the culture medium. We conclude that the terminal guanidino nitrogens of L-arginine are the physiological precursors of endothelium-derived NO.
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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                1660-8151
                2235-3186
                1998
                January 1998
                19 December 1997
                : 78
                : 1
                : 104-111
                Affiliations
                a 2nd Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan; b Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Miss., USA
                Article
                44889 Nephron 1998;78:104–111
                10.1159/000044889
                9453411
                © 1998 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: 4, References: 32, Pages: 8
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/44889
                Categories
                Original Paper

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