Characteristics of apical Cl-HCO3 exchanger of bicarbonate-secreting cells in turtle bladder.

Characteristics of apical Cl-HCO3 exchanger of bicarbonate-secreting cells in turtle bladder.
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龟膀胱碳酸氢盐分泌细胞顶端 Cl-HCO3 交换特性。

DOI:
10.1152/ajprenal.1990.258.1.f9
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发表时间:
1990
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Steinmetz,PR
Steinmetz,PR
中科院分区:
--
文献类型:
--
作者:
Kohn,OF;Mitchell,PP;Steinmetz,PR

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β-碳酸酐酶(CA)细胞的顶端阴离子交换器与α-细胞的基底外侧交换器不同,其对二磺酸芪的敏感性降低,并且缺乏与红细胞带3蛋白抗体的免疫反应性。为了表征交换器,我们检查了葡萄糖酸盐、Br-、SO 4(2-)和NO3-对Cl-的替代以及1)乙酰唑胺(ACZ)(有和没有用叠氮化钠(NaN 3)预处理)、2)呋塞米和3)α-氰基-4-羟基肉桂酸(CHC)的抑制对电中性碳酸氢盐分泌(JHCO 3 n)的影响。Cl-依赖性JHCO 3 n为0.90 +/- 0.09 mumol/h,与ACZ可降解速率0.83 +/- 0.08 mumol/h相似,Cl的表观Km接近3.4 mM。最大JHCO 3 n在管腔pH 6.8和4.5时相当。与氯化物溶液中的速率相比,JHCO 3 n在Br-中降低至约21%,在SO 4(2-)中降低至13%,在NO3-溶液中降低至7%。ACZ抑制没有取消预处理与NaN 3。JHCO 3 n仅被呋塞米轻微抑制(14%),而不被CHC抑制。总之,顶端交换器对氯化物具有选择性,对抑制剂具有相对抗性。它对腔氯化物的依赖性如此之大,以至于其转运速率在浓度低于20 mM时受到粘膜氯化物的密切调节。
The apical anion exchanger of the beta-carbonic anhydrase (CA) cells differs from the basolateral exchanger of the alpha-cells by reduced sensitivity to disulfonic stilbenes and lack of immunoreactivity with antibodies to erythrocyte band 3 protein. To characterize the exchanger, we examined the effects on electroneutral bicarbonate secretion (JHCO3n) of Cl- replacement by gluconate, Br-, SO4(2-), and NO3- and of inhibition by 1) acetazolamide (ACZ) with and without pretreatment with sodium azide (NaN3), 2) furosemide, and 3) alpha-cyano-4-hydroxycinnamate (CHC). The Cl-dependent JHCO3n was 0.90 +/- 0.09 mumol/h, similar to the ACZ-inhibitable rate of 0.83 +/- 0.08 mumol/h with an apparent Km for Cl near 3.4 mM. Maximal JHCO3n was comparable at luminal pH 6.8 and 4.5. JHCO3n was reduced to approximately 21% in Br-, 13% in SO4(2-), and 7% in NO3- solutions compared with the rates in chloride solutions. ACZ inhibition was not abolished by pretreatment with NaN3. JHCO3n was only slightly inhibited (14%) by furosemide and not inhibited by CHC. In conclusion, the apical exchanger is selective for chloride and relatively resistant to inhibitors. Its dependence on luminal chloride is such that its transport rate is closely regulated by mucosal chloride at concentrations below 20 mM.