Kamikawa Y, Shimo Y
Br J Pharmacol. 1983 Jan;78(1):103-10. doi: 10.1111/j.1476-5381.1983.tb09368.x.
1 The site of action of 5-hydroxytryptamine (5-HT) was examined on the isolated muscularis mucosae attached to the submucous plexus of the guinea-pig oesophagus. Isotonic responses of the longitudinal muscularis mucosae were recorded.2 5-HT produced a transient contraction of the muscularis mucosae at concentrations higher than 3 muM. The contraction was rapid in onset, reaching a peak in about 15 s or less, and was restored to the basal level after 20 to 30 s without washing out 5-HT. When the 5-HT-induced contraction faded to the basal tone, successive applications of 5-HT no longer produced any contracture.3 Nicotine (Nic), at concentrations higher than 10 muM, also produced a transient contraction which had a very similar pattern to that induced by 5-HT. Again, the successive application of Nic no longer produced any contracture following prior treatment with Nic itself. However, the 5-HT-induced contraction was not modified by the presence of Nic.4 Exogenously applied acetylcholine (ACh) produced a concentration-dependent contraction of the muscularis mucoase, the 50% effective concentration (EC(50)) was 69 +/- 5.6 nM. The contraction was sustained during incubation with ACh, and was not modified by prior treatment with 5-HT or Nic.5 The 5-HT (100 muM)-induced contraction was completely abolished by tetrodotoxin (0.2 muM) and atropine (0.2 muM). This means that the action is mediated by stimulating cholinergic nerves in the submucous plexus attached to muscularis mucosae. Moreover, the stimulating action of 5-HT does not involve nicotinic receptors, since the action was not blocked by hexamethonium (100 muM).6 Among several 5-MT antagonists examined, methysergide (1 muM), ketanserin (1 muM) and morphine (100 muM) failed to modify the 5-HT (100 muM)-induced contraction significantly. Cinanserin (0.1-3 muM), cyproheptadine (3-100 nM) and phenoxybenzamine (0.1-3 muM) inhibited the 5-HT-induced contraction, in a concentration-dependent manner, and each highest concentration abolished the response. However, none of these antagonists was specific for 5-HT, but the Nic (100 muM) or ACh (0.1 muM)-induced contractions were also inhibited by them.7 The present results indicate that 5-HT contracts the muscularis mucosae of the guinea-pig oesophagus indirectly by stimulating cholinergic nerves in the submucous plexus, and has no direct action on the muscularis mucosae. In addition, the type of 5-HT receptors responsible for the stimulant action may be different from those in other parts of the gastrointestinal tract, blood vessels or brain, because of the different effects of 5-HT antagonists.
研究了5-羟色胺(5-HT)对附着于豚鼠食管黏膜下丛的离体黏膜肌层的作用部位。记录了纵行黏膜肌层的等张反应。
浓度高于3μM时,5-HT可使黏膜肌层产生短暂收缩。收缩起始迅速,约15秒或更短时间内达到峰值,且在不冲洗5-HT的情况下,20至30秒后恢复至基础水平。当5-HT诱导的收缩消退至基础张力时,连续应用5-HT不再产生任何挛缩。
浓度高于10μM时,尼古丁(Nic)也可产生短暂收缩,其模式与5-HT诱导的非常相似。同样,在先用Nic自身处理后,连续应用Nic不再产生任何挛缩。然而,Nic的存在并未改变5-HT诱导的收缩。
外源性应用乙酰胆碱(ACh)可使黏膜肌层产生浓度依赖性收缩,50%有效浓度(EC(50))为69±5.6 nM。与ACh孵育期间收缩持续存在,且不受5-HT或Nic预处理的影响。
5-HT(100μM)诱导的收缩被河豚毒素(0.2μM)和阿托品(0.2μM)完全消除。这意味着该作用是通过刺激附着于黏膜肌层的黏膜下丛中的胆碱能神经介导的。此外,5-HT的刺激作用不涉及烟碱受体,因为该作用未被六甲铵(100μM)阻断。
在几种检测的5-MT拮抗剂中,麦角新碱(1μM)、酮色林(1μM)和吗啡(100μM)未能显著改变5-HT(100μM)诱导的收缩。辛那色林(0.1 - 3μM)、赛庚啶(3 - 100 nM)和酚苄明(0.1 - 3μM)以浓度依赖性方式抑制5-HT诱导的收缩,且每种最高浓度均消除了反应。然而,这些拮抗剂均对5-HT无特异性,它们也抑制Nic(100μM)或ACh(0.1μM)诱导的收缩。
目前的结果表明,5-HT通过刺激黏膜下丛中的胆碱能神经间接使豚鼠食管黏膜肌层收缩,对黏膜肌层无直接作用。此外,由于多种5-HT拮抗剂的不同作用效果,负责刺激作用的5-HT受体类型可能与胃肠道、血管或脑的其他部位不同。