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      Accumulation of 3H-Adrenaline by Rabbit Aorta


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          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

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          23 September 2008
          : 22
          : 1
          : 32-46
          Department of Pharmacology, School of Medicine, Odense University, Denmark
          158582 Blood Vessels 1985;22:32–46
          © 1985 S. Karger AG, Basel

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          Pages: 15
          Research Paper


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