Bicarbonate secretion in interlobular ducts from guinea-pig pancreas
Bicarbonate secretion in interlobular ducts from guinea-pig pancreas
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DOI：
10.1113/jphysiol.1996.sp021583
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发表时间：
1996-08-15
影响因子：
5.5
通讯作者：
Case, RM
中科院分区：
文献类型：
--
作者：
Ishiguro, H;Steward, MC;Case, RM
1.在离体的豚鼠小叶间导管上显微注射细胞外荧光探针--葡聚糖偶联物（BCECF-dextran），通过监测管腔pH值，研究了HCO_3 ~-跨膜转运。在显微注射6-甲氧基-N-（4-氨基烷基）溴化喹啉鎓（ABQ-葡聚糖）和Cl-NERF（Cl-NERF-葡聚糖）的葡聚糖缀合物后，还通过显微荧光测定法测量管腔Cl-浓度。当HCO 3-/CO2进入浴中时，观察到导管腔的短暂酸化，随后是明显的碱化。后者被废除时，管腔Cl-浓度降低到25-35 mM的葡萄糖醛酸和可能取代。因此，应归因于腔膜上的Cl--HCO 3-交换。促胰液素，毛喉素和乙酰胆碱刺激HCO 3-分泌到管腔中，即使当管腔Cl-浓度降低到约7 mM。此外，激动剂诱发的HCO 3-分泌不抑制管腔格列本脲，二氢-4，4 '-二异硫氰基芪-2，2'-二磺酸（H2 DIDS）或5-硝基-2-（3-苯基丙基氨基）-苯甲酸（NPPB）。这些观察结果不容易与跨腔膜的HCO 3-转运相一致，该转运由与Cl-电导平行的Cl--HCO 3-交换介导。4.从水浴中去除Na+可阻断激动剂刺激的HCO 3-分泌，但加入N-甲基-N-异丁基阿米洛利（MIA）或巴弗洛霉素A则不能阻断（1）。这支持了我们先前的结论，即HCO 3-从细胞外液进入导管细胞需要Na+，但不依赖于Na+-H+交换或液泡型H+-ATP酶活性。在这篇文章和随附的论文中描述了胰泌素对豚鼠胰管细胞的三种作用-刺激相对Cl-不敏感的管腔HCO 3-外排途径，刺激基底外侧Na+-HCO 3-共转运，以及缺乏对细胞内pH的影响-需要修改目前的胰腺HCO 3-分泌模型。
1. The transport of HCO3- across the luminal membrane of pancreatic duct cells was studied by monitoring the luminal pH of isolated guinea-pig interlobular ducts after microinjection of an extracellular fluoroprobe, the dextran conjugate of 2'7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF-dextran). Luminal Cl- concentration was also measured by microfluorometry following microinjection of the dextran conjugates of 6-methoxy-N-(4-aminoalkyl)quinolinium bromide (ABQ-dextran) and Cl-NERF (Cl-NERF-dextran).2. When HCO3-/CO2 was admitted to the bath, a transient acidification of the duct lumen was observed, followed by a marked alkalinization. The latter was abolished when the luminal Cl- concentration was reduced to 25-35 mM by replacement with glucuronate and may. therefore, be attributed to Cl--HCO3- exchange at the luminal membrane.3. Secretin, forskolin and acetylcholine stimulated HCO3- secretion into the lumen even when the luminal Cl- concentration was reduced to approximately 7 mM. Furthermore, agonist-evoked HCO3- secretion was not inhibited by luminal glibenclamide, dihydro-4,4'diisothiocyanostilbene-2,2'-disulphonic acid (H2DIDS) or 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB). These observations are not easily reconciled with HCO3- transport across the luminal membrane being mediated by Cl--HCO3- exchange in parallel with a Cl- conductance. 4. Agonist-stimulated HCO3- secretion was blocked by omitting Na+ from the bath but not by addition of N-methyl-N-isobutylamiloride (MIA) or bafilomycin A(1). This supports our previous conclusion that HCO3- entry into duct cells from the extracellular fluid requires Na+ but is not dependent on Na+-H+ exchange or vacuolar-type H+-ATPase activity.5. The three actions of secretin on guinea-pig pancreatic duct cells described in this and the accompanying paper - stimulation of a relatively Cl--insensitive luminal HCO3- efflux pathway, stimulation of basolateral Na+-HCO3- cotransport, and lack of effect on intracellular pH - require the current model of pancreatic HCO3- secretion to be modified.