The inhibitory action of noradrenaline and adrenaline on acetylcholine output by guinea‐pig ileum longitudinal muscle strip
The inhibitory action of noradrenaline and adrenaline on acetylcholine output by guinea‐pig ileum longitudinal muscle strip
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去甲肾上腺素和肾上腺素对豚鼠回肠纵肌条乙酰胆碱输出的抑制作用
DOI：
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发表时间：
1969
影响因子：
7.3
通讯作者：
E. Vizi
中科院分区：
文献类型：
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作者：
W. Paton;E. Vizi
1在静息状态和刺激后，去甲肾上腺素和肾上腺素可使豚鼠回肠纵条的乙酰胆碱输出减少80%。该效应随剂量而分级，用去甲肾上腺素2 × 10−7 g/ml即可检测到。肾上腺素的活性大约是去甲肾上腺素的4倍，并且其作用在被洗脱后更持久。2如果静息输出高，两种胺具有成比例的更大的作用，并且随着剂量的增加，它们的作用是将静息输出降低到基础水平，相对恒定的从一条到另一条，约为10 ng/g/min。3在刺激下，当每次截击的输出高时，胺的作用在低频下比在高频下更大。通过增加所传递的冲击的数量来降低该效果。因此，似乎存在1-2 ng/g/volley数量级的每一次抽射的基础输出，这可以通过相对快速的刺激、通过延长的刺激或通过用这些胺处理来达到。[4]如果在40/min的持续刺激期间应用去甲肾上腺素，则在其存在期间乙酰胆碱输出的抑制之后，当药物被撤回时，输出增加。这种“过冲”的幅度随着去甲肾上腺素暴露的持续时间而增加。5去氧肾上腺素4 μg/ml。苯丙胺20 μg/ml。异丙肾上腺素1 μg/ml，多巴胺1 μg/ml。和甲氧胺10 μg/ml。是无效的。6.酚苄明减少静息输出，增加刺激输出。其他两个阻断剂检查，酚妥拉明没有影响，无论是休息或刺激输出和麦角胺短暂减少刺激输出。酚苄明的作用不是由于与肾上腺素受体或毒蕈碱受体的反应。7.酚苄明、酚妥拉明和麦角胺可消除肾上腺素和去甲肾上腺素对静息输出和刺激反应输出的影响。[8]在用利血平和乙啶处理过的动物的脑条中，发现静息乙酰胆碱输出和低频刺激输出增加，在这些条件下，去甲肾上腺素仍然有效。9通过对氯苯丙氨酸处理降低试纸的羟色胺含量并不显著影响乙酰胆碱的输出。[10]由此得出结论，由纵带神经网络输出的乙酰胆碱在交感神经的正常控制下，通过α受体介导的一种突触前抑制。这意味着，对于处于双重自主控制下的组织，交感神经控制的撤销将导致副交感神经反应，其不仅不受对抗，而且本身也被增强。
1 Noradrenaline and adrenaline reduce the output of acetylcholine by the guinea‐pig ileum longitudinal strip by up to 80%, both in resting conditions and after stimulation. The effect is graded with dose, and is detectable with noradrenaline 2 × 10−7 g/ml. Adrenaline is approximately 4 times as active as noradrenaline, and its action after being washed out is more persistent. 2 If resting output is high, both amines have a proportionately greater effect and their action, as dosage is increased, is to reduce resting output to a basal level, relatively constant from strip to strip, of about 10 ng/g/min. 3 With stimulation, the effect of the amine is greater at low frequencies, when the output per volley is high, than at high frequencies. The effect is reduced by increasing the number of shocks delivered. There thus appears to be a basal output per volley, of the order of 1–2 ng/g/volley, which can be reached either by relatively rapid stimulation, by prolonged stimulation, or by treatment with these amines. 4 If noradrenaline is applied during continued stimulation at 40/min, the depression of acetylcholine output during its presence is followed by an augmented output when the drug is withdrawn. The magnitude of this “overshoot” increases with the duration of noradrenaline exposure. 5 Phenylephrine 4 μg/ml. and amphetamine 20 μg/ml. reduced the acetylcholine output, but isoprenaline 1 μg/ml., dopamine 1 μg/ml. and methoxamine 10 μg/ml. were ineffective. 6 Phenoxybenzamine reduced the resting output and increased the stimulation output. Of the two other blocking agents examined, phentolamine had no effect on either resting or stimulation output and ergotamine transiently reduced stimulation output. The effect of phenoxybenzamine was not due to a reaction with either adrenoceptive or muscarinic receptors. 7 Phenoxybenzamine, phentolamine and ergotamine abolished the effect of adrenaline and noradrenaline on both resting output and on output in response to stimulation. 8 In strips obtained from animals treated with reserpine and guanethidine, a rise in resting acetylcholine output and in stimulation output at low frequencies was found. In these conditions, noradrenaline was still effective. 9 Reducing the hydroxytryptamine content of the strips by treatment with p‐chloro‐(±)‐phenylalanine did not significantly affect acetylcholine output. 10 It is concluded that acetylcholine output by the nervous networks of the longitudinal strip is under the normal control of the sympathetic by a species of presynaptic inhibition mediated by α receptors. This implies that for a tissue under dual autonomic control, withdrawal of sympathetic control will lead to a parasympathetic response which is not only unopposed but also itself enhanced.