体外青蛙胃黏膜中钠依赖的氢离子和氯离子转运

Na+-dependent H+ and Cl- transport in in vitro frog gastric mucosa.

作者信息

Machen T E, McLennan W L

出版信息

Am J Physiol. 1980 May;238(5):G403-13. doi: 10.1152/ajpgi.1980.238.5.G403.

DOI:10.1152/ajpgi.1980.238.5.G403

Abstract

Na+ dependency of H+ and Cl- transport in resting and stimulated gastric mucosae was investigated. We measured transepithelial potential difference (PD), short-circuit current (Isc), conductance, H+ secretion (JH), and unidirectional fluxes of 36Cl- (muscosal (m) to serosal (s), JClm leads to s and JCLs leads to m) during Isc conditions in Ussing-type chambers. Resting tissues: Na+-free serosal solution (choline replacement), but not mucosal, Ringer solution caused PD and Isc to decrease to zero with a time course identical to that observed with Cl--free solutions. Conductance also decreased by more than 50%. Isc = JCLs leads to m--JCLm leads to 8 = JClnet during control ([Na+] = 105 mM), and Na+-free conditions. When [Na+] = 50 mM (choline replacement) Isc (=JClnet) was reduced by approximately 25%; when K+ replaced Na+, Isc (=JClnet) was reduced by approximately 65%. The dependence of Isc on [Na+] (choline replacement) was sigmoidal indicating that there may be two sites at which Na+ activates Cl- secretion. Plots of 1/Isc vs. 1/[Cl-] with different [NA+] indicated, that the affinity of the Cl- "carrier" may be affected by [Na+]. stimulated tissues: Na+-free (choline replacement) solutions caused PD, Isc, and JClnet all to decrease to zero but sometimes Na+-containing mucosal solution caused JH to increase back to 50% of control, whereas Isc increased by only 16%. Na+-free effects were not reversed by 1 mM dibutyryl cAMP plus 0.1 mM isobutyl methylxanthine in the serosal solution. As [Na+] was increased, Isc (sigmoidal) and JH (monotonic) both increased. K+ replacement of Na+ caused a larger decrease in Isc than when choline was used; JH remained constant if [Na+] greater than or equal to mM. We have proposed that the energy-dependent step for active Cl- transport occurs at the serosal membrane in a Na+-coupled process. Cl- that accompanies JH during open-circuit conditions may utilize a separate system.

摘要

研究了静息和刺激状态下胃黏膜中H⁺和Cl⁻转运对Na⁺的依赖性。我们在Ussing型小室的短路电流（Isc）条件下，测量了跨上皮电位差（PD）、短路电流（Isc）、电导、H⁺分泌（JH）以及³⁶Cl⁻的单向通量（从黏膜（m）到浆膜（s），JClm→s和JCLs→m）。静息组织：无Na⁺的浆膜溶液（用胆碱替代），而非黏膜林格溶液，会使PD和Isc随时间降至零，其时间进程与无Cl⁻溶液时观察到的相同。电导也下降超过50%。在对照（[Na⁺]=105 mM）和无Na⁺条件下，Isc = JCLs→m - JCLm→s = JClnet。当[Na⁺]=50 mM（用胆碱替代）时，Isc（=JClnet）降低约25%；当K⁺替代Na⁺时，Isc（=JClnet）降低约65%。Isc对[Na⁺]（用胆碱替代）的依赖性呈S形，表明可能有两个Na⁺激活Cl⁻分泌的位点。不同[Na⁺]条件下1/Isc对1/[Cl⁻]的作图表明，Cl⁻“载体”的亲和力可能受[Na⁺]影响。刺激组织：无Na⁺（用胆碱替代）溶液会使PD、Isc和JClnet均降至零，但有时含Na⁺的黏膜溶液会使JH回升至对照的50%，而Isc仅增加16%。浆膜溶液中1 mM二丁酰环磷腺苷加0.1 mM异丁基甲基黄嘌呤不能逆转无Na⁺的效应。随着[Na⁺]增加，Isc（呈S形）和JH（呈单调变化）均增加。K⁺替代Na⁺比用胆碱时导致Isc下降幅度更大；如果[Na⁺]≥ mM，JH保持不变。我们提出，主动Cl⁻转运的能量依赖步骤发生在浆膜，是一个与Na⁺偶联的过程。开路条件下伴随JH的Cl⁻可能利用一个独立系统。