Bicarbonate transport by rabbit duodenum in vitro: effect of vasoactive intestinal polypeptide, prostaglandin E2, and cyclic adenosine monophosphate.
Bicarbonate transport by rabbit duodenum in vitro: effect of vasoactive intestinal polypeptide, prostaglandin E2, and cyclic adenosine monophosphate.
复制标题
体外兔十二指肠的碳酸氢盐转运：血管活性肠多肽、前列腺素 E2 和环磷酸腺苷的作用。
DOI：
10.1016/0016-5085(93)91008-6
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发表时间：
1993
期刊：
影响因子：
29.4
通讯作者：
Isenberg,JI
中科院分区：
文献类型：
--
作者：
Yao,B;Hogan,DL;Bukhave,K;Koss,MA;Isenberg,JI
背景：十二指肠表面细胞分泌碳酸氢盐，为损伤提供屏障。本实验旨在确定十二指肠重碳酸盐的调节和转运途径。方法：在短路条件下，将兔十二指肠近端粘膜固定在小室中。测定前列腺素E_2(PGE_2)、血管活性肠肽(VIP)和环磷酸二丁酯(db-cAMP)对碳酸氢盐转运、短路电流(ISC)和电位差(PD)的影响。结果：前列腺素E_2、血管活性肠肽、db-cAMP和茶碱能显著增加十二指肠细胞分泌−、胰岛素敏感性和PD。哇巴因、无钠洗澡溶液和缺氧(N_2)可抑制这些反应。DIDS和无氯−溶液可阻断前列腺素E_2诱导的反应，使对血管活性肠肽的反应减少约50%，对db-cAMP的反应无影响。结论：哺乳动物十二指肠HCO3−转运需要依赖Na+，Na+/K+-腺苷三磷酸酶和O2依赖的代谢途径，并受PGE2、VIP和cAMP的刺激，作用途径不同。
Background:Duodenal surface cells secrete bicarbonate that provides a barrier against injury. The current experiments were performed to identify duodenal bicarbonate regulatory and transport pathways.Methods:Rabbit proximal duodenal mucosa were mounted in chambers under short-circuited conditions. Bicarbonate transport, short-circuit current (Isc), and potential difference (PD) were quantitated in response to prostaglandin E2(PGE2), vasoactive intestinal polypeptide (VIP), and dibutyryl cyclic adenosine monophosphate (db-cAMP). Anoxia (N2), 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS) and Cl−free solutions, ouabain, and Na-free solutions were also studied, as was the effect of VIP and PGE2on duodenocyte cAMP.Results:PGE2, VIP, db-cAMP, and theophylline significantly increased bicarbonate secretion, Isc, and PD. Ouabain, Na+-free bathing solutions, and anoxia (N2) inhibited the responses. DIDS and Cl−-free solutions abolished the PGE2-induced response, reduced the response to VIP by about 50%, and had no effect on the response to db-cAMP. After PGE2and VIP, cAMP concentration increased, yet was likely independent of bicarbonate secretion.Conclusions:Mammalian duodenal HCO3−transport requires Na+, Na+/K+-adenosine triphospatase and O2-dependent metabolic pathways and is stimulated by PGE2, VIP, and cAMP, acting by distinct pathways.