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      Enhanced Dendroaspis Natriuretic Peptide Immunoreactivity in Experimental Ureteral Obstruction

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          Abstract

          Whether the postobstructive diuresis can in part be related to an altered regulation of Dendroaspis natriuretic peptide (DNP) was investigated. Male Sprague-Dawley rats were bilaterally obstructed of their ureters. Control group was with sham ureteral obstruction. Forty-eight h later, tissue levels of DNP immunoreactivity were determined in the plasma, heart, and kidneys. Urine samples were collected in some rats under anesthesia. The plasma DNP immunoreactivity was significantly increased by 45% in the experimental group. The tissue levels of DNP immunoreactivity in the atrium, ventricle, or kidneys did not significantly differ between the experimental and control groups. The urinary flow and sodium excretion rate were 3- to 4-fold increased in the experimental group. The urinary DNP excretion was also increased in the experimental group, which was positively correlated with the urinary volume and sodium excretion. The urinary excretion of cGMP was 2- to 3-fold increased in the experimental group. These results indicate that an enhanced DNP activity may in part be causally related to the postobstructive diuresis.

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          Mechanism of relaxations to dendroaspis natriuretic peptide in canine coronary arteries.

          Experiments were designed to determine mechanisms by which Dendroaspis natriuretic peptide (DNP) causes relaxations in coronary arteries. Rings of canine left circumflex artery with and without endothelium were suspended in organ chambers filled with Krebs-Ringer bicarbonate solution (37 degrees C, bubbled with 95% O2/5% CO2). Concentration-response curves to DNP (10(-10) to 3 x 10(-7) M) were obtained in arteries contracted with prostaglandin (PGF(2alpha), 2 x 10(-6) M), either in the absence or the presence of C-ANP (10(-6) M) to inhibit natriuretic clearance receptors; indomethacin to inhibit cyclooxygenase (INDO, 10(-5) M), N(G)-monomethyl-L-arginine to inhibit production of nitric oxide (L-NMMA; 10(-4) M), HS-142-1 to inhibit particulate guanylate cyclase (10(-5) M); 1H-[1,2,4]oxadiazolo-[4,3-alpha]quinoxalin-1-one to inhibit soluble guanylate cyclase (ODQ; 10(-5) M), or tetraethylammonium to inhibit potassium channels (TEA; 10(-3) or 10(-2) M). Relaxations to DNP were greater in rings with than in those without endothelium. C-ANP significantly attenuated relaxations to DNP only in rings with endothelium. HS-146-1 but not INDO, L-NMMA, ODQ, and TEA significantly reduced relaxations to DNP in rings with and without endothelium contracted with PGF(2alpha). These results suggest that the endothelium augments inhibitory effects of DNP and that natriuretic clearance receptors mediate this component of the response to DNP in canine coronary arteries. In addition, relaxations to DNP in canine arterial smooth muscle involve activation of particulate guanylate cyclase but not hyperpolarization.
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            Author and article information

            Journal
            NEF
            Nephron
            10.1159/issn.1660-8151
            Nephron
            S. Karger AG
            1660-8151
            2235-3186
            2002
            October 2002
            02 September 2002
            : 92
            : 2
            : 369-372
            Affiliations
            aDepartment of Physiology and Research Institute of Medical Sciences, Chonnam National University Medical School, Gwangju; bDepartment of Physiology, Chonbuk University School of Medicine, Jeonju, Korea
            Article
            63302 Nephron 2002;92:369–372
            10.1159/000063302
            12218316
            © 2002 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: 16, Pages: 4
            Product
            Self URI (application/pdf): https://www.karger.com/Article/Pdf/63302
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