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      L-Arginine Availability Is Not Limiting for Nitric Oxide Generation from Recombinant Endothelial Nitric Oxide Synthase

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          Abstract

          L-Arginine (L-Arg) may be limiting for inducible nitric oxide synthase (NOS) activity and under certain circumstances, such as increased concentrations of a NOS inhibitor, may also be limiting for endothelial NOS activity. It is unknown if L-Arg is limiting for recombinant eNOS activity in the vascular wall after adenoviral mediated gene transfer. Our aim was to examine, if L-Arg is limiting for recombinant eNOS activity in the normal or atherosclerotic vessel wall. Rings of rabbit aorta from chow or cholesterol fed animals were transduced with adenovirus vector encoding eNOS (AdeNOS) or β-galactosidase (AdβGal). After 24 h, transgene expression was confirmed and vasomotor studies were performed in the absence or presence of L-Arg. During maximal contractions to phenylephrine (10<sup>–5</sup>  M), L-Arg (3 m M) was added to the organ chamber for 30 min. Subsequently, relaxations to acetylcholine during half-maximal contractions were obtained. In the chow- and cholesterol-fed animals, relaxations were significantly enhanced in the NOS and NOS + L-Arg groups compared to the βGal and βGal + L-Arg groups. There was no difference between NOS and NOS + L-Arg or βGal and βGal + L-Arg rings from chow- or cholesterol-fed animals. While gene transfer of eNOS enhances endothelium-dependent vasorelaxation in the normal and atherosclerotic vessel wall, L-arginine is not limiting for recombinant eNOS activity.

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          Particulate systems and polymers for in vitro and in vivo delivery of polynucleotides

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            Author and article information

            Journal
            JVR
            J Vasc Res
            10.1159/issn.1018-1172
            Journal of Vascular Research
            S. Karger AG
            1018-1172
            1423-0135
            1999
            December 1999
            24 December 1999
            : 36
            : 6
            : 437-444
            Affiliations
            Division of Endocrinology, Metabolism, and Internal Medicine, Mayo Clinic and Foundation, Rochester, Minn., USA
            Article
            25686 J Vasc Res 1999;36:437–444
            10.1159/000025686
            10629419
            © 1999 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: 5, Tables: 2, References: 37, Pages: 8
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