Matsushima Yohkazu, Muto Shigeaki, Taniguchi Junichi, Imai Masashi
Department of Cardiovascular Dynamics, Research Institute, National Cardiovascular Center, Osaka, Japan.
Clin Exp Nephrol. 2006 Jun;10(2):102-10. doi: 10.1007/s10157-006-0417-8.
Pendrin, an anion exchanger known to participate in iodide transport in the apical membrane of follicular cells of the thyroid gland, has recently been shown to exist in the apical membrane of the beta- and gamma-intercalated (beta/gamma-IC) cells of the cortical collecting duct (CCD). We examined mechanisms of iodide transport in the CCD.
Rabbit CCD was perfused in vitro, and lumen-to-bath flux coefficients for both (125)I(-) (K(I (lb))) and (36)Cl(-) (K(Cl (lb))) were measured simultaneously. The intracellular pH (pHi) of beta/gamma-IC cells in the perfused CCD was measured by microscopic fluorometory, by loading 2',7'-bis-(2-carboxyethyl)-5(6)-carboxyfluorescein tetraacetoxy methylester (BCECF-AM), a fluorescent marker for pHi. The effects on pHi of the replacement of NaCl with Na cyclamate, NaI, or NaBr in the lumen or bath were observed.
K(I (lb)) was comparable to or slightly higher than K(Cl (lb)). Both iodide and chloride in the lumen caused self- and cross-inhibitions to both fluxes. The addition of 5-nitro-2-(-3-phenylpropylamino)-benzoate (NPPB), a Cl(-) channel inhibitor, to the bath significantly reduced K(Cl (lb)), but not K(I (lb)). Replacement of luminal fluid NaCl with Na cyclamate, NaI, or NaBr caused alkalization of pHi, no change in pHi, and slight acidification of pHi, respectively. Replacement of bath NaCl with Na cyclamate, NaI, or NaBr caused alkalization, alkalization, and acidification of pHi, respectively. Luminal NaI prevented the acidification of pHi caused by bath Na cyclamate.
The data are consistent with the model that iodide is transported via the Cl(-)/HCO(3) (-) exchanger in the apical membrane of beta/gamma-IC cells and exits the basolateral membrane via an electroneutral transporter that is distinct from the Cl(-) channel. We could not, however, identify which type of beta/gamma-IC cell was mainly responsible.
Pendrin是一种阴离子交换蛋白，已知其参与甲状腺滤泡细胞顶膜中的碘转运，最近研究表明它存在于皮质集合管（CCD）的β和γ闰细胞（β/γ-IC）的顶膜中。我们研究了CCD中碘转运的机制。
对兔CCD进行体外灌注，同时测量¹²⁵I⁻（K（I（lb）））和³⁶Cl⁻（K（Cl（lb）））的管腔到浴液的通量系数。通过显微荧光测定法测量灌注的CCD中β/γ-IC细胞的细胞内pH（pHi），方法是加载2',7'-双（2-羧乙基）-5（6）-羧基荧光素四乙酰氧基甲酯（BCECF-AM），这是一种用于pHi的荧光标记物。观察了用环己基氨基磺酸钠、碘化钠或溴化钠替代管腔或浴液中的氯化钠对pHi的影响。
K（I（lb））与K（Cl（lb））相当或略高。管腔中的碘化物和氯化物对两种通量都有自我抑制和交叉抑制作用。向浴液中添加5-硝基-2-（-3-苯丙基氨基）-苯甲酸酯（NPPB），一种Cl⁻通道抑制剂，可显著降低K（Cl（lb）），但不影响K（I（lb））。用环己基氨基磺酸钠、碘化钠或溴化钠替代管腔液中的氯化钠分别导致pHi碱化、pHi无变化和pHi轻微酸化。用环己基氨基磺酸钠、碘化钠或溴化钠替代浴液中的氯化钠分别导致pHi碱化、碱化和酸化。管腔中的碘化钠可防止浴液中环己基氨基磺酸钠引起的pHi酸化。
这些数据与碘化物通过β/γ-IC细胞顶膜中的Cl⁻/HCO₃⁻交换体转运并通过一种与Cl⁻通道不同的电中性转运体从基底外侧膜排出的模型一致。然而，我们无法确定哪种类型的β/γ-IC细胞起主要作用。
