Plasma membrane H(+)-HCO3- transport in rat hepatocytes: a principal role for Na(+)-coupled HCO3- transport.
Plasma membrane H(+)-HCO3- transport in rat hepatocytes: a principal role for Na(+)-coupled HCO3- transport.
复制标题
大鼠肝细胞质膜 H( )-HCO3- 转运：Na( )-耦合 HCO3- 转运的主要作用。
DOI：
10.1152/ajpgi.1991.261.5.g803
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Scharschmidt,BF
中科院分区：
文献类型：
--
作者：
Fitz,JG;Lidofsky,SD;Xie,MH;Cochran,M;Scharschmidt,BF
Na（+）-偶联HCO 3-转运已在肝细胞的基底外侧膜中得到证实，但与其他H（+）-HCO 3-转运机制相比，其化学计量或能力尚不确定。在无Na+的培养基中预孵育后，无论是否存在HCO 3（-）-CO2，将原代培养的大鼠肝细胞重新暴露于Na+或HCO 3（-）-CO2单独或组合。通过测量膜电位差（PD）评估转运蛋白的产电性，并通过使用BCECF测量细胞内pH（pHi）的变化幅度和速率评估Na（+）-偶联HCO 3-转运、Cl（-）-HCO 3-交换和Na（+）-H+交换的相对能力。在不存在Na+的情况下，单独暴露于HCO 3-对PD或pHi没有一致的影响。无HCO_3 ~-时，Na ~+使细胞去极化3 ± 1 mV，使pHi增加0.031 ± 0.02units/min，而有HCO_3 ~-时，Na ~+使细胞超极化-14 ± 5 mV，使pHi增加0.133 ± 0.11units/min; SITS抑制超极化和碱化，而阿米洛利不影响。PD的这些变化表明Na（+）-偶联HCO 3-转运是产电的，与一个以上的HCO 3-与每个Na+偶联一致。此外，SITS可激活的Na（+）依赖的碱化作用超过阿米洛利可激活的Na（+）依赖的碱化作用一个数量级，表明Na（+）耦合的HCO 3-转运能力超过Na（+）-H+交换。（250字处删节）
Na(+)-coupled HCO3- transport has been demonstrated in the basolateral membrane of hepatocytes, but there is uncertainty regarding its stoichiometry or capacity compared with other mechanisms of H(+)-HCO3- transport. After preincubation in medium free of Na+, either in the presence or absence of HCO3(-)-CO2, rat hepatocytes in primary culture were reexposed to Na+ or HCO3(-)-CO2 alone or in combination. Transporter electrogenicity was assessed by measuring membrane potential difference (PD), and the relative capacities of Na(+)-coupled HCO3- transport, Cl(-)-HCO3- exchange, and Na(+)-H+ exchange were assessed by measuring the magnitude and rate of change of intracellular pH (pHi) using BCECF. In the absence of Na+, exposure to HCO3- alone had no consistent effect on PD or pHi. In the absence of HCO3-, reexposure to Na+ depolarized cells by 3 +/- 1 mV and caused an amiloride-inhibitable increase in pHi of 0.031 +/- 0.02 units/min. In the presence of HCO3-, reexposure to Na+ hyperpolarized cells by -14 +/- 5 mV and increased pHi at a rate of 0.133 +/- 0.11 units/min; both the hyperpolarization and alkalinization were inhibited by SITS but unaffected by amiloride. These changes in PD indicate that Na(+)-coupled HCO3- transport is electrogenic, consistent with coupling of more than one HCO3- to each Na+. Furthermore, SITS-inhibitable Na(+)-dependent alkalinization exceeds amiloride-inhibitable Na(+)-dependent alkalinization by an order of magnitude, suggesting that the transport capacity of Na(+)-coupled HCO3- transport exceeds that of Na(+)-H+ exchange.(ABSTRACT TRUNCATED AT 250 WORDS)