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      Does Nitric Oxide Regulate Smooth Muscle Cell Proliferation?

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          Abstract

          Smooth muscle proliferation is involved in the pathogenesis of atherosclerosis, restenosis after angioplasty and vein graft failure due to neointimal hyperplasia. Nitric oxide (NO) inhibits smooth muscle cell growth in vitro and experimental neointimal hyperplasia in vivo, suggesting a role for NO as a regulator of smooth muscle cell proliferation. NO is also involved in the control of numerous other vascular functions including platelet and inflammatory cell adhesion, vascular reactivity and endothelial permeability. This review critically examines the experimental and clinical evidence that supports a role for NO as a modulator of smooth muscle cell proliferation, with an emphasis on the multiple mechanisms by which NO acts on vascular lesions.

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          Correction of endothelial dysfunction in coronary microcirculation of hypercholesterolaemic patients by L-arginine

          H Just, H Drexler, A.M Zeiher … (1991)
          Article 0 comments Cited 59 times – based on 0 reviews     Review now
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            p53 expression in nitric oxide-induced apoptosis.

            M Ankarcrona, P Nicotera, B Brüne … (1994)
            Nitric oxide (NO) is a diffusible messenger involved in several patho-physiological processes including immune-mediated cytotoxicity and neural cell killing. NO or the products of its redox chemistry can cause DNA damage and activate subsequent lethal reactions including energy depletion and cell necrosis. However, regardless of whether it is endogenously produced in response to cytokines, or generated by chemical breakdown of donor molecules, NO can also induce apoptosis in different systems. Here, we report that NO generation in response to a cytokine induced NO-synthase or by NO donors stimulates the expression of the tumor suppressor gene, p53, in RAW 264.7 macrophages or pancreatic RINm5F cells prior to apoptosis. NO-synthase inhibitors such as NG-monomethyl-L-arginine prevent the inducible NO generation as well as p53 expression and apoptosis. Since p53 expression is linked to apoptosis in some cells exposed to DNA damaging agents, we suggest that NO-induced apoptosis in these cell systems is the consequence of DNA damage and subsequent expression of this tumor suppressor gene.
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              L-Arginine Inhibits Balloon Catheter-Induced Intimal Hyperplasia

              D.B. Mcnamara, L.J. Ignarro, L Tena … (1993)
              Intimal hyperplasia that results from therapeutic revascularization is an important etiologic factor in the failure of these procedures (i.e., restenosis). Drugs which donate nitric oxide have been shown to inhibit the proliferation of vascular smooth muscle cells in vitro. We tested the hypothesis that administration of L-arginine (0.5 g/kg/day), the precursor of nitric oxide, would inhibit development of intimal hyperplasia following balloon catheter-induced injury. L-arginine administration from 2 days prior to and 2 weeks following catheter-induced injury to the rabbit thoracic aorta attenuated the development of intimal hyperplasia by 39% as compared with untreated controls. This effect was due to decreased intimal area. The effect of L-arginine was inhibited by co-administration of an inhibitor of nitric oxide synthase, NG-nitro-L-arginine methyl ester (0.5 g/kg/day). These data demonstrate that L-arginine attenuates intimal hyperplasia and suggest that the mechanism for this effect is the conversion of L-arginine to nitric oxide.
              Article 0 comments Cited 12 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (publisher-id): JVR
                Journal ID (nlm-ta): J Vasc Res
                Journal ID (doi): 10.1159/issn.1018-1172
                Title: Journal of Vascular Research
                Publisher: S. Karger AG
                ISSN (Print): 1018-1172
                ISSN (Electronic): 1423-0135
                Publication date Subscription-year: 1998
                Publication date (Print): June 1998
                Publication date (Electronic): 09 June 1998
                Volume: 35
                Issue: 3
                Pages: 135-142
                Affiliations
                a Department of Surgery, University of California (Los Angeles) Medical Center, Los Angeles, Calif., and b Department of Physiology, University of Michigan Medical School, Ann Arbor, Mich., USA
                Article
                Publisher ID: 25576 Other ID: J Vasc Res 1998;35:135–142
                DOI: 10.1159/000025576
                PubMed ID: 9647326
                SO-VID: 8b42f9be-0317-44b9-9718-159e038cbbd5
                Copyright © © 1998 S. Karger AG, Basel
                License:

                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.

                History
                Page count
                Figures: 2, References: 69, Pages: 8
                Categories
                Subject: Review

                ScienceOpen disciplines: General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
                Keywords: Arginine,Vasodilators,Atherosclerosis,Balloon angioplasty,Restenosis,Endothelium
                Data availability:
                ScienceOpen disciplines: General medicine, Neurology, Cardiovascular Medicine, Internal medicine, Nephrology
                Keywords: Arginine, Vasodilators, Atherosclerosis, Balloon angioplasty, Restenosis, Endothelium

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