Effect of 5-hydroxytryptamine on duodenal mucosal bicarbonate secretion in mice.
Effect of 5-hydroxytryptamine on duodenal mucosal bicarbonate secretion in mice.
复制标题
5-羟色胺对小鼠十二指肠粘膜碳酸氢盐分泌的影响。
DOI：
10.1016/s0016-5085(03)01045-x
复制
发表时间：
2003
期刊：
影响因子：
29.4
通讯作者：
Isenberg,JonI
中科院分区：
文献类型：
--
作者：
Tuo,Bi-Guang;Isenberg,JonI
背景与目的5-羟色胺（5-HT）是一种重要的神经递质和细胞间信使，调节多种胃肠功能。由于很少有人知道的作用，5-羟色胺在调节十二指肠碳酸氢盐的分泌，我们研究了5-羟色胺对十二指肠碳酸氢盐的分泌的作用，并定义神经通路参与的行动5-HT.MethodsDuodenal粘膜从美国国立卫生研究院瑞士小鼠被剥离的浆肌层和安装在Ussing室。用pH法测定5-HT对十二指肠碳酸氢盐分泌的影响。结果血清浴中加入5-HT可明显刺激十二指肠碳酸氢盐分泌和短路电流（Isc），并呈剂量依赖性（10 - 7 ~ 10 - 3 mol/L; P < 0.0001），而粘膜加入5-HT则无此作用。5-HT刺激的碳酸氢盐分泌不依赖于管腔Cl−。用河豚毒素（TTX）（10− 6 mol/L）或阿托品（10− 5 mol/L）预处理可显著降低5-HT刺激的十二指肠碳酸氢盐分泌（分别降低60%和65%; P < 0.001）和Isc（分别降低45%和27%; P < 0.001和P < 0.05）。用Nω-硝基-l-精氨酸甲酯（l-NAME）（10− 3 mol/L）、普萘洛尔（10− 5 mol/L）或酚妥拉明（10− 5 mol/L）预处理，未显著改变5-HT刺激的十二指肠粘膜碳酸氢盐分泌或Isc。5-HT浓度依赖性地诱发十二指肠粘膜ACh释放（P < 0.0001）。TTX可显著抑制5-HT诱导的ACh释放（P < 0.001）。结论5-HT是一种有效的十二指肠粘膜碳酸氢盐分泌的激活剂。5-HT在体外诱导的十二指肠碳酸氢盐分泌主要通过胆碱能神经通路发生。
Background & Aims5-hydroxytryptamine (5-HT) is an important neurotransmitter and intercellular messenger that modulates many gastrointestinal functions. Because little is known about the role of 5-HT in the regulation of duodenal bicarbonate secretion, we examined the role of 5-HT on duodenal bicarbonate secretion and define neural pathways involved in the actions of 5-HT.MethodsDuodenal mucosa from National Institutes of Health Swiss mice was stripped of seromuscular layers and mounted in Ussing chambers. The effect of 5-HT on duodenal bicarbonate secretion was determined by the pH stat technique. Acetylcholine (ACh) release from duodenal mucosa was assessed by preincubating the tissue with [3H] choline and measuring 5-HT-evoked release of tritium.Results5-HT added to the serosal bath markedly stimulated duodenal bicarbonate secretion and short circuit current (Isc) in a dose-dependent manner (10−7mol/L to 10−3mol/L; P < 0.0001), whereas mucosally added 5-HT was without effect. 5-HT—stimulated bicarbonate secretion was independent of luminal Cl−. Pretreatment with tetrodotoxin (TTX) (10−6mol/L) or atropine (10−5mol/L) markedly reduced 5-HT—stimulated duodenal bicarbonate secretion (by 60% and 65%, respectively; P < 0.001) and Isc (by 45% and 27%, respectively; P < 0.001 and P < 0.05). Pretreatment with Nω-nitro-l-arginine methyl ester (l-NAME) (10−3mol/L), propranolol (10−5mol/L), or phentolamine (10−5mol/L) did not significantly alter 5-HT—stimulated duodenal mucosal bicarbonate secretion or Isc. 5-HT concentration-dependently evoked ACh release from duodenal mucosal preparations (P < 0.0001). TTX markedly inhibited 5-HT-evoked ACh release (P < 0.001).Conclusions5-HT is a potent activator of duodenal mucosal bicarbonate secretion in mice. Duodenal bicarbonate secretion induced by 5-HT in vitro occurs principally via a cholinergic neural pathway.