Different responsiveness of excitatory and inhibitory enteric motor neurons in the human esophagus to electrical field stimulation and to nicotine

Different responsiveness of excitatory and inhibitory enteric motor neurons in the human esophagus to electrical field stimulation and to nicotine
复制标题

DOI:
10.1152/ajpgi.00534.2003
复制
发表时间:
2004-07-01
影响因子:
4.5
通讯作者:
Clavé, P
Clavé, P
中科院分区:
医学2区
文献类型:
--
作者:
González, AA;Farré, R;Clavé, P

文献摘要

被引文献

相似文献

为比较电场刺激(EFS)和尼古丁对人食道内兴奋性和抑制性肠运动神经元(EMN)的兴奋和抑制作用,在器官浴中研究了20例人的食管环、下括约肌(LES)、环状和纵向食管体(EB)条。比较基础条件下,N-G-硝基-L-精氨酸(L-NNA;100um)、L-NNA和阿帕明(1um)对EFS或尼古丁(100um)的反应。TTX(5微米)或L-NNA可增强LES条的肌张力。TTX可取消EFS-LES的松弛,不受六甲溴铵(100um)的影响,但可被阿托品(3um)增强。尼古丁-LES松弛高于EFS松弛,被TTX或阿托品降低,并被六甲溴铵阻断。L-NNA后,EFS在环状LES和EB上引起强烈的胆碱能收缩,尼古丁在LES上引起少量的收缩,在EB上没有收缩作用。L-NNA和阿帕明后,EFS引起LES和EB强烈的胆碱能收缩,尼古丁引起的弱收缩分别为EFS的6.64+/-3.19和9.20+/-5.51%。EFS引起纵条收缩;L-NNA和阿帕明作用后,尼古丁不引起任何反应。抑制性肌动蛋白抑制肌源性LES张力,并可被位于躯体树突和神经末梢的EFS和烟碱型乙酰胆碱受体(NAChRs)有效地刺激,释放一氧化氮和一种对阿帕明敏感的神经递质。相反,虽然EFS能有效地刺激食道兴奋性eMN,但其通过nAChRs的刺激是困难的,并且引起微弱的反应,提示非烟碱机制参与了人食道兴奋性eMN的神经传递。
To compare electrical field stimulation (EFS) with nicotine in the stimulation of excitatory and inhibitory enteric motoneurons (EMN) in the human esophagus, circular lower esophageal sphincter (LES), and circular and longitudinal esophageal body (EB) strips from 20 humans were studied in organ baths. Responses to EFS or nicotine (100 muM) were compared in basal conditions, after N-G-nitro-L-arginine (L-NNA; 100 muM), and after L-NNA and apamin (1 muM). LES strips developed myogenic tone enhanced by TTX (5 muM) or L-NNA. EFS-LES relaxation was abolished by TTX, unaffected by hexamethonium ( 100 muM), and enhanced by atropine (3 muM). Nicotine-LES relaxation was higher than EFS relaxation, reduced by TTX or atropine, and blocked by hexamethonium. After L-NNA, EFS elicited a strong cholinergic contraction in circular LES and EB, and nicotine elicited a small relaxation in LES and no contractile effect in EB. After L-NNA and apamin, EFS elicited a strong cholinergic contraction in LES and EB, and nicotine elicited a weak contraction amounting to 6.64 +/- 3.19 and 9.20 +/- 5.51% of that induced by EFS. EFS elicited a contraction in longitudinal strips; after L-NNA and apamin, nicotine did not induce any response. Inhibitory EMN tonically inhibit myogenic LES tone and are efficiently stimulated both by EFS and nicotinic acetylcholine receptors (nAChRs) located in somatodendritic regions and nerve terminals, releasing nitric oxide and an apamin-sensitive neurotransmitter. In contrast, although esophageal excitatory EMN are efficiently stimulated by EFS, their stimulation through nAChRs is difficult and causes weak responses, suggesting the participation of nonnicotinic mechanisms in neurotransmission to excitatory EMN in human esophagus.