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      Accumulation of 3H-Adrenaline by Rabbit Aorta

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          Abstract

          The accumulation of (–)<sup>-3</sup>H-adrenaline (<sup>3</sup>H-A) by rabbit isolated aorta was studied. In all experiments, monoamine oxidase and catechol-O-methyltransferase were inhibited by treatment with pargyline and 3’,4’-dihydroxy-2-methyl-propiophenone (U-0521), respectively. The relationship between the accumulation of <sup>3</sup>H derived from <sup>3</sup>H-A (10<sup>–8</sup> M) and the duration of incubation (0–3 h) was linear. The <sup>3</sup>H-accumulation after 3 h incubation was 22.5 ml·g<sup>-1</sup>. In reserpine-treated tissue, the <sup>3</sup>H-accumulation levelled off after 30 min and was 8.5 ml·g<sup>–1</sup> after 3 h. The concentration of <sup>3</sup>H-A or (–)<sup>-3</sup>H-noradrenaline (<sup>3</sup>H-NA) and the <sup>3</sup>H-accumulation (ml·g<sup>–1</sup>) were inversely related. At 10<sup>–8</sup> M, the 1-hour accumulation of <sup>3</sup>H derived from <sup>3</sup>H-A and <sup>3</sup>H-NA was 7.8 and 15.2 ml·g<sup>–1</sup>, respectively. With increasing concentrations (3 × 10<sup>–8</sup>–10<sup>–4</sup> M), the accumulation values approached each other. At 10<sup>–4</sup> M, the accumulation was 2.3 and 2.8 ml·g<sup>-1</sup> for <sup>3</sup>H-A and <sup>3</sup>H-NA, respectively. The accumulation of <sup>3</sup>H derived from <sup>3</sup>H-A (10<sup>–8</sup>–10<sup>–4</sup> M) by reserpine-treated tissue also showed an inverse relationship with concentration: 5.4 ml·g<sup>-1</sup> (10<sup>–8</sup> M) and 2.6 ml·g<sup>–1</sup> (10–4 Af). The accumulation of <sup>3</sup>H derived from <sup>3</sup>H-A (10–8 M; 1 h) was dependent on the bath temperature (1–37 °C). The accumulation increased continuously from 1.1 ml·g<sup>–1</sup> (1 °C) to 11.1 ml·g<sup>-1</sup> (37 °C). Storage of tissue (0–5 days in salt solution without equilibration with 95% O<sub>2</sub>/5% CO<sub>2</sub>; 4 °C) did not affect the accumulation of <sup>3</sup>H derived from <sup>3</sup>H-A (10<sup>–8</sup> M; 1 h). Thereafter (7–14 days), the accumulation decreased. The inhibitory potency (IC<sub>5o</sub>; –log M) of desimipramine, cocaine, (–)-propranolol, (–)-isoprenaline, and (±)-normetanephrine on accumulation of <sup>3</sup>H derived from <sup>3</sup>H-A (10<sup>-8</sup> M; 1 h) was found to be 8.26; 6.50; 5.48, 4.88, and 4.02, respectively. The maximal degree of inhibition was almost the same for these drugs, while that of clonidine and corticosterone was 50 and 20%, respectively. In the presence of desimipra-mine (10<sup>–6</sup> M), either clonidine (10<sup>–5</sup>–10<sup>–3</sup> M), corticosterone (10<sup>–6</sup>–10<sup>–4</sup> M) or (-)-isoprena-line (10<sup>–5</sup>–10<sup>–3</sup> M) reduced the accumulation of <sup>3</sup>H derived from <sup>3</sup>H-A (10<sup>–8</sup> M; 1 h). Oua-bain (3 × 10<sup>–4</sup> M) and iodoacetic acid (10<sup>–3</sup> M), but not sodium cyanide (10<sup>–3</sup> M) and 2,4-dinitrophenol (10<sup>–3</sup> M), reduced the accumulation of <sup>3</sup>H derived from <sup>3</sup>H-A (10<sup>–8</sup> M; 1 h). Anoxia (95% N<sub>2</sub>/5% CO<sub>2</sub>; 37 °C; 1–24 h) did not alter the accumulation of <sup>3</sup>H derived from <sup>3</sup>H-A (10<sup>–8</sup> M; 1 h). D-(+)-Glucose deprivation alone or combined with anoxia markedly reduced the <sup>3</sup>H-accumulation. These results suggest that adrenaline is transported into neu-ronal and extraneuronal sites via a carrier mechanism which is energy-dependent.

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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
          1985
          1985
          23 September 2008
          : 22
          : 1
          : 32-46
          Affiliations
          Department of Pharmacology, School of Medicine, Odense University, Denmark
          Article
          158582 Blood Vessels 1985;22:32–46
          10.1159/000158582
          © 1985 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
          Pages: 15
          Categories
          Research Paper

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