Reimann W
Arzneimittelforschung. 1984;34(5):575-8.
Rabbit pulmonary artery strips were used for the evaluation of the alpha 1-/alpha 2-agonistic activity of norfenefrine (active principle of the antihypotensive agent Novadral) and for the investigation of neuronal uptake and release mechanisms for norfenefrine in the vessel wall. At 0.1 and 1 mumol/l, norfenefrine caused contractions of the artery strips, while presynaptic inhibition of stimulation-evoked noradrenaline release could not be detected with certainty. Thus, in the range tested, alpha 1-agonistic activity was more pronounced. Uptake and release of 3H-norfenefrine was studied on noradrenaline-depleted arteries. Rabbits were pretreated either with alpha-methyl-p-tyrosine (metirosine, alpha-MT) to inhibit noradrenaline synthesis without affecting storage vesicle function or with reserpine to eliminate vesicular storage capacity. In arteries from animals pretreated with alpha-MT, more substance was retained after preincubation with 3H-norfenefrine, in comparison with reserpine pretreated arteries, and about 2% of the substance was released from Arteries from reserpine pretreated animals retained less 3H-norfenefrine after preincubation, in comparison with alpha-MT pretreated arteries, and less than 0.2% was released per stimulation period. After alpha-MT treatment, tension developed upon stimulation was enhanced after norfenefrine preincubation, while contractions of reserpine pretreated arteries were independent of norfenefrine preincubation. These results provide evidence for an uptake of norfenefrine in the noradrenaline storage vesiculation period. After alpha-MT treatment, tension developed upon stimulation was enhanced after norfenefrine preincubation, while contractions of reserpine pretreated arteries were independent of norfenefrine preincubation. These results provide evidence for an uptake of norfenefrine in the noradrenaline storage vesicles and a vesicular co-secretion of norfenefrine with noradrenaline upon stimulation. The impaired sympathetic transmission was thereby improved.
兔肺动脉条用于评估去甲麻黄碱（抗低血压药物诺瓦得然的活性成分）的α1-/α2-激动活性，并研究去甲麻黄碱在血管壁中的神经元摄取和释放机制。在0.1和1μmol/L浓度下，去甲麻黄碱引起动脉条收缩，但无法确定其对刺激诱发的去甲肾上腺素释放的突触前抑制作用。因此，在所测试的范围内，α1-激动活性更为明显。在去甲肾上腺素耗竭的动脉上研究了3H-去甲麻黄碱的摄取和释放。兔子分别用α-甲基对酪氨酸（美替拉酮，α-MT）预处理以抑制去甲肾上腺素合成而不影响储存囊泡功能，或用利血平预处理以消除囊泡储存能力。与利血平预处理的动脉相比，用α-MT预处理的动物的动脉在与3H-去甲麻黄碱预孵育后保留了更多的物质，并且约2%的物质从利血平预处理动物的动脉中释放出来。与α-MT预处理的动脉相比，利血平预处理的动脉在预孵育后保留的3H-去甲麻黄碱较少，并且每个刺激周期释放的物质少于0.2%。α-MT处理后经去甲麻黄碱预孵育后刺激时产生的张力增强，而利血平预处理的动脉收缩与去甲麻黄碱预孵育无关。这些结果为去甲麻黄碱在去甲肾上腺素储存囊泡期的摄取提供了证据。α-MT处理后经去甲麻黄碱预孵育后刺激时产生的张力增强，而利血平预处理的动脉收缩与去甲麻黄碱预孵育无关。这些结果为去甲麻黄碱在去甲肾上腺素储存囊泡中的摄取以及刺激时去甲麻黄碱与去甲肾上腺素的囊泡共同分泌提供了证据。由此改善了受损的交感神经传递。
