Liedtke C M, Hopfer U
Am J Physiol. 1982 Mar;242(3):G272-80. doi: 10.1152/ajpgi.1982.242.3.G272.
The mechanisms of Cl- transport across the brush-border membrane from rat small intestine were investigated in vitro in isolated vesicles and in vivo in ileal and jejunal segments. A Cl--OH- exchange mechanism was demonstrated in isolated vesicles by observing concentrative Cl- uptake driven by a pH gradient (extravesicular pH less than intravesicular pH). A Cl- conductance pathway was demonstrated by concentrative Cl- uptake driven by a K+ diffusion potential. The K+ diffusion potential was generated by a K+ concentration gradient in the presence of valinomycin (extravesicular K+ concentration greater than intravesicular K+ concentration). Furosemide and stilbene 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonate (SITS) strongly inhibited the Cl--OH- exchange but did not affect the Cl- conductance pathway, Na+-dependent glucose transport, and Na+-Na+ exchange. Under isotope exchange conditions at equilibrium, SITS inhibited Cl- transport up to 63%, indicating that this portion of Cl- transport is mediated by the Cl--OH- exchange transporter, with the remainder presumably due to the Cl- conductance pathway. In perfused small intestinal segments, Na+, Cl-, HCO3(-), and water were absorbed from the lumen in the absence of SITS. The presence of 5 mM SITS inhibited NaCl absorption and decreased HCO3(-) and water absorption in both jejunum and ileum but did not affect glucose absorption. The inhibition of in vivo salt absorption by SITS suggests that the Cl--OH- exchange mechanism plays a major role in NaCl absorption in intact enterocytes.
在体外分离的囊泡以及体内回肠和空肠段中，对大鼠小肠刷状缘膜上氯离子（Cl⁻）转运机制进行了研究。通过观察由pH梯度（囊泡外pH低于囊泡内pH）驱动的Cl⁻浓缩摄取，在分离的囊泡中证实了一种Cl⁻-OH⁻交换机制。通过由钾离子（K⁺）扩散电位驱动的Cl⁻浓缩摄取，证实了一种Cl⁻传导途径。K⁺扩散电位是在缬氨霉素存在下由K⁺浓度梯度产生的（囊泡外K⁺浓度大于囊泡内K⁺浓度）。呋塞米和芪类化合物4-乙酰氨基-4'-异硫氰酸芪-2,2'-二磺酸盐（SITS）强烈抑制Cl⁻-OH⁻交换，但不影响Cl⁻传导途径、钠依赖性葡萄糖转运和钠-钠交换。在平衡状态下的同位素交换条件下，SITS抑制Cl⁻转运高达63%，表明这部分Cl⁻转运是由Cl⁻-OH⁻交换转运体介导的，其余部分可能归因于Cl⁻传导途径。在灌注的小肠段中，在没有SITS的情况下，Na⁺、Cl⁻、HCO₃⁻和水从肠腔被吸收。5 mM SITS的存在抑制了NaCl吸收，并降低了空肠和回肠中HCO₃⁻和水的吸收，但不影响葡萄糖吸收。SITS对体内盐吸收的抑制表明，Cl⁻-OH⁻交换机制在完整肠细胞的NaCl吸收中起主要作用。
