人类十二指肠近端的碱性分泌是由Cl⁻/HCO₃⁻交换和HCO₃⁻传导介导的。

Human proximal duodenal alkaline secretion is mediated by Cl-/HCO3- exchange and HCO3- conductance.

作者信息

Nyberg L, Pratha V, Hogan D L, Rapier R C, Koss M A, Isenberg J I

机构信息

Division of Gastroenterology, UCSD Medical Center, University of California San Diego, 92103, USA.

出版信息

Dig Dis Sci. 1998 Jun;43(6):1205-10. doi: 10.1023/a:1018895405362.

DOI:10.1023/a:1018895405362

PMID:9635609

Abstract

The proximal duodenal epithelium secretes bicarbonate into an adherent mucus layer, thereby protecting the mucosa from injury by gastric acid and pepsin. While bicarbonate secretion is stimulated and inhibited by a number of agonists and antagonists, the apical anion transport pathways have not been addressed fully. The objective was to assess if apical Cl-/HCO3- exchange and Cl-:HCO3- conductance are involved in duodenal mucosal bicarbonate secretion (DMBS). In healthy volunteers, the proximal 4 cm of duodenum was isolated, perfused with either saline or 4,4'-diisothiocyano-2,2'-disulfonic acid (DIDS), and bicarbonate secretion and transepithelial potential difference (PD) were stimulated by either PGE2 or the phosphodiesterase inhibitor theophylline to increase cyclic AMP. Luminal DIDS abolished PGE2-stimulated DMBS, yet had no effect on the increase in PD and failed to significantly alter theophylline-induced DMBS and PD. Therefore, in human proximal duodenum, it appears that PGE2 and cAMP activate distinct HCO3- transport pathways likely involving a DIDS-sensitive Cl-/HCO3- exchanger and DIDS-insensitive HCO3- conductance.

摘要

十二指肠近端上皮细胞向附着的黏液层分泌碳酸氢盐，从而保护黏膜免受胃酸和胃蛋白酶的损伤。虽然多种激动剂和拮抗剂可刺激或抑制碳酸氢盐分泌，但顶端阴离子转运途径尚未得到充分研究。本研究旨在评估顶端Cl⁻/HCO₃⁻交换和Cl⁻:HCO₃⁻电导是否参与十二指肠黏膜碳酸氢盐分泌（DMBS）。在健康志愿者中，分离十二指肠近端4 cm，分别用生理盐水或4,4'-二异硫氰酸-2,2'-二磺酸（DIDS）灌注，并用前列腺素E2（PGE2）或磷酸二酯酶抑制剂茶碱刺激碳酸氢盐分泌和跨上皮电位差（PD）以增加环磷酸腺苷（cAMP）。腔内DIDS消除了PGE2刺激的DMBS，但对PD的增加没有影响，也未显著改变茶碱诱导的DMBS和PD。因此，在人十二指肠近端，PGE2和cAMP似乎激活了不同的HCO₃⁻转运途径，可能涉及一种对DIDS敏感的Cl⁻/HCO₃⁻交换体和对DIDS不敏感的HCO₃⁻电导。