Abrahamsen J
Department of Pharmacology, Odense University, Denmark.
Pharmacol Toxicol. 1991;69 Suppl 3:1-40. doi: 10.1111/j.1600-0773.1991.tb01613.x.
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, respectively. The relationship between the accumulation of 3H derived from 3H-A and the duration of incubation was linear. The 3H-accumulation after 3 h incubation was 22.5 ml/g. In reserpine-treated tissue, the 3H-accumulation levelled off after 30 min and was 8.5 ml/g after 3 h. The concentration of 3H-A or (-)-3H-noradrenaline (3H-NA) and the 3H-accumulation (ml/g) 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, respectively. With increasing concentrations the accumulation values approached each other. The accumulation of 3H derived from 3H-A by reserpine-treated tissue also showed an inverse relationship with concentration. The accumulation of 3H derived from 3H-A was dependent on the bath temperature. Storage of tissue (0-5 days in salt solution without equilibration with 95% O2/5% CO2; 4 degrees C) did not affect the accumulation of 3H derived from 3H-A. Thereafter (7-14 days), the accumulation decreased. The inhibitory potency (IC50; -log M) of desipramine, cocaine, propranolol, isoprenaline, and normetanephrine on accumulation of 3H derived from 3H-A 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 desipramine, either clonidine, corticosterone or isoprenaline reduces the accumulation of 3H derived from 3H-A. Ouabain and iodoacetic acid, but not sodium cyanide and 2,4-dinitrophenol, reduced the accumulation of 3H derived from 3H-A. Anoxia (95% N2/5% CO2; 37 degrees C; 1-24 h) did not alter the accumulation of 3H derived from 3H-A. Glucose deprivation alone or combined with anoxia markedly reduced the 3H-accumulation. The release of 3H-A from rabbit isolated aorta was studied. This release was compared with that of 3H-NA. The stimulation-evoked 3H-overflow from aorta preloaded with 3H-A decreased with repeated stimulation. In contrast, prestimulation enhanced subsequent stimulation-evoked 3H-overflows. For both 3H-amines, the 3H-overflow increased concomitantly to the same degree with the number of pulses. The time course of 3H-overflows with either 3H-A or 3H-NA was compared.(ABSTRACT TRUNCATED AT 400 WORDS)
研究了兔离体主动脉对（-）-3H-肾上腺素（3H-A）的摄取情况。在所有实验中，分别用优降宁和3'，4'-二羟基-2-甲基苯丙酮处理以抑制单胺氧化酶和儿茶酚-O-甲基转移酶。源自3H-A的3H摄取量与孵育时间呈线性关系。孵育3小时后的3H摄取量为22.5 ml/g。在利血平处理的组织中，3H摄取在30分钟后趋于平稳，3小时后为8.5 ml/g。3H-A或（-）-3H-去甲肾上腺素（3H-NA）的浓度与3H摄取量（ml/g）呈负相关。在10（-8）M时，源自3H-A和3H-NA的3H 1小时摄取量分别为7.8和15.2 ml/g。随着浓度增加，摄取值相互接近。利血平处理的组织对源自3H-A的3H摄取也与浓度呈负相关。源自3H-A的3H摄取取决于浴温。组织储存（在盐溶液中0 - 5天，未与95% O2/5% CO2平衡；4℃）不影响源自3H-A的3H摄取。此后（7 - 14天），摄取量下降。发现地昔帕明、可卡因、普萘洛尔、异丙肾上腺素和去甲变肾上腺素对源自3H-A的3H摄取的抑制效力（IC50；-log M）分别为8.26；6.50；5.48；4.88和4.02。这些药物的最大抑制程度几乎相同，而可乐定和皮质酮的分别为50%和20%。在地昔帕明存在的情况下，可乐定、皮质酮或异丙肾上腺素均可降低源自3H-A的3H摄取。哇巴因和碘乙酸可降低源自3H-A的3H摄取，但氰化钠和2,4-二硝基苯酚则不能。缺氧（95% N2/5% CO2；37℃；1 - 24小时）未改变源自3H-A的3H摄取。单独的葡萄糖剥夺或与缺氧联合均显著降低3H摄取。研究了兔离体主动脉中3H-A的释放。将该释放与3H-NA的释放进行了比较。预先用3H-A加载的主动脉经刺激诱发的3H溢出随重复刺激而减少。相反，预刺激增强了随后刺激诱发的3H溢出。对于两种3H胺，3H溢出均随脉冲数同步增加相同程度。比较了3H-A和3H-NA的3H溢出的时间进程。（摘要截断于400字）
