Steward Martin C, Ishiguro Hiroshi, Case R Maynard
Faculty of Life Sciences, University of Manchester, Manchester M13 9PT, United Kingdom.
Annu Rev Physiol. 2005;67:377-409. doi: 10.1146/annurev.physiol.67.031103.153247.
In many species the pancreatic duct epithelium secretes HCO3- ions at a concentration of around 140 mM by a mechanism that is only partially understood. We know that HCO3- uptake at the basolateral membrane is achieved by Na+-HCO3- cotransport and also by a H+-ATPase and Na+/H+ exchanger operating together with carbonic anhydrase. At the apical membrane, the secretion of moderate concentrations of HCO3- can be explained by the parallel activity of a Cl-/HCO3- exchanger and a Cl- conductance, either the cystic fibrosis transmembrane conductance regulator (CFTR) or a Ca2+-activated Cl- channel (CaCC). However, the sustained secretion of HCO3- into a HCO- -rich luminal fluid cannot be explained by conventional Cl-/HCO3- exchange. HCO3- efflux across the apical membrane is an electrogenic process that is facilitated by the depletion of intracellular Cl-, but it remains to be seen whether it is mediated predominantly by CFTR or by an electrogenic SLC26 anion exchanger.
在许多物种中,胰腺导管上皮细胞通过一种仅部分为人所知的机制,以约140 mM的浓度分泌HCO₃⁻离子。我们知道,在基底外侧膜处,HCO₃⁻的摄取是通过Na⁺-HCO₃⁻协同转运以及与碳酸酐酶共同作用的H⁺-ATP酶和Na⁺/H⁺交换体来实现的。在顶端膜处,中等浓度HCO₃⁻的分泌可以通过Cl⁻/HCO₃⁻交换体和Cl⁻电导(囊性纤维化跨膜电导调节因子(CFTR)或Ca²⁺激活的Cl⁻通道(CaCC))的并行活动来解释。然而,HCO₃⁻持续分泌到富含HCO₃⁻的管腔液中无法用传统的Cl⁻/HCO₃⁻交换来解释。HCO₃⁻穿过顶端膜的外流是一个电生成过程,细胞内Cl⁻的消耗会促进该过程,但它是否主要由CFTR或电生成的SLC26阴离子交换体介导仍有待观察。