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      Relative Roles of Nitric Oxide, Prostanoids and Angiotensin II in the Regulation of Canine Glomerular Hemodynamics

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          Abstract

          Glomerular hemodynamics are controlled by a variety of physical, nervous and hormonal factors including the potent vasoconstrictors, angiotensin (ANG) II and endothelin-1 (ET-1), and the vasodilator prostanoids (prostaglandin = PG) and nitric oxide (NO). Since no micropuncture data on the canine kidney exist with respect to the relative roles of the endogenous vasoactive hormones/autacoids NO, PG and ANG II in modulating glomerular hemodynamics, in the present study using the micropuncture technique in anesthetized dogs on a normal salt intake, we investigated the relative effects of these hormones/autacoids by means of the L-arginine analog, N<sup>ω</sup>-nitro- L-arginine methyl ester hydrochloride ( L-NAME), a competitive NO synthase (NOS) inhibitor, the cyclooxygenase inhibitor indomethacin (INDO), and the AT<sub>1</sub> receptor blocker EXP 3174. An intrarenal arterial (i.r.a.) bolus (within 5 min) of 2.5 mg of L-NAME led to a significant decrease in total renal blood flow (RBF) and single nephron glomerular blood flow (SNGBF) from 4.46 ± 0.51 to 3.52 ± 0.41 ml/min/g kidney weight and from 0.393 ± 0.041 to 0.341 ± 0.037 µl/min (p < 0.01), respectively, without a change in glomerular filtration rate (GFR). The increase in arteriolar resistance was more pronounced at the efferent (+31%) than at the afferent (+13%) arteriole, and K<sub>f</sub> decreased from 4.5 ± 0.5 to 3.7 ± 0.4 nl/min/mm Hg (p < 0.01). INDO (5 mg/kg i.v. bolus followed by 0.17 mg/kg/min i.v.) had no effect on glomerular hemodynamics. EXP 3174 (30 µg/kg/min i.r.a.) increased RBF and SNGBF from 4.35 ± 0.45 to 4.99 ± 0.50 ml/min/g kidney weight and from 0.403 ± 0.028 to 0.478 ± 0.039 µl/min (p < 0.01), respectively, without an effect on GFR. It reduced the efferent arteriolar resistance by 25% as compared to 13% at the afferent arteriolar level. EXP 3174 increased K<sub>f</sub> from 5.1 ± 0.4 to 8.1 ± 0.6 mm Hg (p < 0.01) in the presence of a decrease in effective filtration pressure from 13.2 ± 1.7 to 8.3 ± 1.0  mm Hg (p < 0.01). The glomerular hemodynamic effects of L-NAME were unaltered by pretreatment with INDO or EXP 3174, whereas its tubular effects were restored in the presence of EXP 3174. Thus, from these first micropuncture data in the anesthetized dog on a normal sodium intake we conclude that (1) acute intrarenal inhibition of NOS by L-NAME decreases RBF and SNGBF due to vasoconstriction of the afferent and, more pronounced, efferent arterioles. Since L-NAME simultaneously decreases K<sub>f</sub>, GFR remains unaltered. (2) These renal hemodynamic effects of NOS inhibition were not mediated by prostanoids or intrarenal ANG II. Thus, the tonic activity of intrarenal NOS plays an important role in maintaining glomerular hemodynamics in the canine kidney.

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          Endothelin and angiotensin mediate most glomerular responses to nitric oxide inhibition

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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
            2004
            July 2004
            02 February 2004
            : 27
            : 1
            : 10-17
            Affiliations
            aRenal Section, Medical Policlinic, University of Bonn, Bonn, Germany; bDepartment of Experimental Medicine, Institute for Clinical and Experimental Medicine, and cCenter for Experimental Cardiovascular Research, Prague, Czech Republic
            Article
            74551 Kidney Blood Press Res 2004;27:10–17
            10.1159/000074551
            14583658
            © 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: 45, Pages: 8
            Product
            Self URI (application/pdf): https://www.karger.com/Article/Pdf/74551
            Categories
            Original Paper

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