Effect of Cocaine and Corticosterone on the Metabolism of 3H‐Noradrenaline Released from Rabbit Isolated Aorta and Adventitia

Schrold, Jørgen; Nedergaard, Ove A.

doi:10.1111/j.1600-0773.1981.tb01614.x

Cited by 11 publications

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References 23 publications

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“…This agrees with other in vitro experiments with canine saphenous vein Guimaraes et al, 1978], rat uterus [Green and Miller, 1966], rat heart [Iversen, 1965a, b], and guinea-pig vas defer ens [Kaisuragi, 1978], A is a good substrate for both MAO and COMT [Blaschko and Richter, 1937]. MAO and COMT arc present and functional in aorta [Verity et al, 1972;Levin, 1974; Schrold and Nedergaard, 1981;Henseling et al. 1976].…”

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confidence: 77%

Accumulation of 3H-Adrenaline by Rabbit Aorta

Abrahamsen¹,

Nedergaard²

1985

J Vasc Res

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The accumulation of (–)-3H-adrenaline (3H-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 3H derived from 3H-A (10–8 M) and the duration of incubation (0–3 h) was linear. The 3H-accumulation after 3 h incubation was 22.5 ml·g-1. In reserpine-treated tissue, the 3H-accumulation levelled off after 30 min and was 8.5 ml·g–1 after 3 h. The concentration of 3H-A or (–)-3H-noradrenaline (3H-NA) and the 3H-accumulation (ml·g–1) were inversely related. At 10–8 M, the 1-hour accumulation of 3H derived from 3H-A and 3H-NA was 7.8 and 15.2 ml·g–1, respectively. With increasing concentrations (3 × 10–8–10–4 M), the accumulation values approached each other. At 10–4 M, the accumulation was 2.3 and 2.8 ml·g-1 for 3H-A and 3H-NA, respectively. The accumulation of 3H derived from 3H-A (10–8–10–4 M) by reserpine-treated tissue also showed an inverse relationship with concentration: 5.4 ml·g-1 (10–8 M) and 2.6 ml·g–1 (10–4 Af). The accumulation of 3H derived from 3H-A (10–8 M; 1 h) was dependent on the bath temperature (1–37 °C). The accumulation increased continuously from 1.1 ml·g–1 (1 °C) to 11.1 ml·g-1 (37 °C). Storage of tissue (0–5 days in salt solution without equilibration with 95% O2/5% CO2; 4 °C) did not affect the accumulation of 3H derived from 3H-A (10–8 M; 1 h). Thereafter (7–14 days), the accumulation decreased. The inhibitory potency (IC5o; –log M) of desimipramine, cocaine, (–)-propranolol, (–)-isoprenaline, and (±)-normetanephrine on accumulation of 3H derived from 3H-A (10-8 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 (10–6 M), either clonidine (10–5–10–3 M), corticosterone (10–6–10–4 M) or (-)-isoprena-line (10–5–10–3 M) reduced the accumulation of 3H derived from 3H-A (10–8 M; 1 h). Oua-bain (3 × 10–4 M) and iodoacetic acid (10–3 M), but not sodium cyanide (10–3 M) and 2,4-dinitrophenol (10–3 M), reduced the accumulation of 3H derived from 3H-A (10–8 M; 1 h). Anoxia (95% N2/5% CO2; 37 °C; 1–24 h) did not alter the accumulation of 3H derived from 3H-A (10–8 M; 1 h). D-(+)-Glucose deprivation alone or combined with anoxia markedly reduced the 3H-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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