肠神经系统调节哺乳动物十二指肠黏膜碳酸氢盐分泌。

The enteric nervous system modulates mammalian duodenal mucosal bicarbonate secretion.

作者信息

Hogan D L, Yao B, Steinbach J H, Isenberg J I

机构信息

Division of Gastroenterology, University of California, San Diego.

出版信息

Gastroenterology. 1993 Aug;105(2):410-7. doi: 10.1016/0016-5085(93)90714-n.

DOI:10.1016/0016-5085(93)90714-n

PMID:8335196

Abstract

BACKGROUND

Interaction of the enteric nerves in regulating mammalian duodenal mucosal bicarbonate secretion is not well understood. The purpose of the present experiments was to evaluate the role of the enteric nervous system on bicarbonate secretion from rabbit duodenal mucosa in vitro.

METHODS

Proximal duodenum from male New Zealand White rabbits was stripped of seromuscular layers, mounted in Ussing chambers, and studied under short-circuited conditions. Effects of electrical field stimulation, vasoactive intestinal polypeptide (VIP), carbachol, prostaglandin E2 (PGE2), dibutyryl-cyclic adenosine monophosphate (db-cAMP), and the neurotoxin tetrodotoxin (TTX) and muscarinic blockade by atropine were studied.

RESULTS

Electrical field stimulation significantly (P < 0.01) stimulated bicarbonate secretion, short-circuit current (Isc), and electrical potential difference (PD) that was sensitive to both TTX and atropine. VIP-stimulated bicarbonate secretion was significantly inhibited by TTX (-73%), yet Isc and PD remained unchanged. Atropine decreased VIP-induced bicarbonate secretion (-69%) and Isc (-43%). Carbachol-stimulated bicarbonate secretion, Isc, and PD were abolished by atropine, whereas TTX was without affect. Neither TTX nor atropine had a significant effect on PGE2 or db-cAMP-stimulated bicarbonate secretion.

CONCLUSIONS

These results suggest that (1) enteric nerve stimulation activates an acetylcholine receptor that in turn stimulates duodenal epithelial bicarbonate secretion; (2) VIP stimulates bicarbonate secretion, in large part, via the enteric nervous system; and (3) PGE2 and cAMP stimulate bicarbonate secretion independent of the enteric nervous system.

摘要

背景

肠道神经在调节哺乳动物十二指肠黏膜碳酸氢盐分泌中的相互作用尚未完全明确。本实验的目的是评估肠道神经系统对兔十二指肠黏膜碳酸氢盐分泌的作用。

方法

取雄性新西兰白兔的近端十二指肠，去除浆膜肌层，安装在尤斯灌流小室中，在短路条件下进行研究。研究了电场刺激、血管活性肠肽（VIP）、卡巴胆碱、前列腺素E2（PGE2）、二丁酰环磷酸腺苷（db-cAMP）以及神经毒素河豚毒素（TTX）和阿托品对毒蕈碱的阻断作用。

结果

电场刺激显著（P < 0.01）刺激了碳酸氢盐分泌、短路电流（Isc）和对TTX和阿托品均敏感的电位差（PD）。TTX显著抑制了VIP刺激的碳酸氢盐分泌（-73%），但Isc和PD保持不变。阿托品降低了VIP诱导的碳酸氢盐分泌（-69%）和Isc（-43%）。卡巴胆碱刺激的碳酸氢盐分泌、Isc和PD被阿托品消除，而TTX无影响。TTX和阿托品对PGE2或db-cAMP刺激的碳酸氢盐分泌均无显著影响。