Marshall I, Nasmyth P A, Shepperson N B
Br J Pharmacol. 1978 Sep;64(1):145-51. doi: 10.1111/j.1476-5381.1978.tb08651.x.
1 The effects of endogenous noradrenaline released by tyramine and the influence of depletion of the tissue noradrenaline with reserpine and/or alpha-methyl-p-tyrosine on the twitch responses of the field-stimulated mouse vas deferens have been studied.2 Tyramine (10-40 muM) inhibited the twitch responses to field stimulation and failed to produce a contraction. The inhibition decreased as the rate of stimulation increased.3 The inhibition produced by tyramine was antagonized by cocaine (10 muM) and by yohimbine (10 nM), which indicated that it was produced by released noradrenaline acting on presynaptic alpha-adrenoceptors.4 Depletion of the tissue noradrenaline by 39% by blockade of the synthesis of noradrenaline with alpha-methyl-p-tyrosine, was without effect on the twitch response but it reduced the inhibitory effect of tyramine.5 Depletion of the tissue noradrenaline by 96.5% with reserpine alone and by 99.4%, with a combination of reserpine and alpha-methyl-p-tyrosine, reduced the twitch responses by approximately 66% and virtually abolished the inhibition produced by tyramine. It also increased the rate of decline of the responses when the tissue was continuously stimulated. The remaining twitch was not antagonized by phenoxybenzamine (15 muM).6 Residual twitches were bigger in tissues depleted by 99.4% than in those depleted by only 96.5%. This difference was eliminated in the presence of yohimbine (128 nM).7 It is concluded that inhibition of the twitch responses by tyramine is produced by stimulation of presynaptic alpha-adrenoceptors and that the twitch response is associated with stimulation of the sympathetic neurone, but that it is not mediated by postsynaptic alpha-adrenoceptors.
1 研究了酪胺释放的内源性去甲肾上腺素的作用，以及利血平和/或α-甲基对酪氨酸耗竭组织去甲肾上腺素对场刺激小鼠输精管抽搐反应的影响。
2 酪胺（10 - 40μM）抑制场刺激的抽搐反应，且未能引起收缩。随着刺激频率增加，抑制作用减弱。
3 酪胺产生的抑制作用被可卡因（10μM）和育亨宾（10 nM）拮抗，这表明它是由释放的去甲肾上腺素作用于突触前α-肾上腺素受体产生的。
4 用α-甲基对酪氨酸阻断去甲肾上腺素合成使组织去甲肾上腺素耗竭39%，对抽搐反应无影响，但降低了酪胺的抑制作用。
5 单独使用利血平使组织去甲肾上腺素耗竭96.5%，利血平和α-甲基对酪氨酸联合使用使组织去甲肾上腺素耗竭99.4%，抽搐反应分别降低约66%，并几乎消除了酪胺产生的抑制作用。当组织持续受到刺激时，还增加了反应的下降速率。剩余的抽搐反应不被苯氧苄胺（15μM）拮抗。
6 去甲肾上腺素耗竭99.4%的组织中的残余抽搐比仅耗竭96.5%的组织中的更大。在育亨宾（128 nM）存在下，这种差异消失。
7 得出结论：酪胺对抽搐反应的抑制是由突触前α-肾上腺素受体的刺激产生的，抽搐反应与交感神经元的刺激有关，但不是由突触后α-肾上腺素受体介导的。
