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

Na+-dependent H+ and Cl- transport in in vitro frog gastric mucosa.
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体外青蛙胃粘膜中 Na 依赖性 H 和 Cl 转运。

DOI:
10.1152/ajpgi.1980.238.5.g403
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发表时间:
1980
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
W. L. McLennan
W. L. McLennan
中科院分区:
--
文献类型:
--
作者:
T. Machen;W. L. McLennan

文献摘要

被引文献

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本文研究了静息和刺激胃粘膜H ~+和Cl ~-转运的Na ~+依赖性。我们测量了跨上皮电位差(PD),短路电流(Isc),电导,H+分泌(JH),和单向流量的36 Cl-(muscosal(m)serenal(s),JClm导致s和JCLs导致m)在Isc条件下在Ussing型室。静息组织:不含Na+的seroglycan溶液(胆碱替代),但不是粘膜,林格氏溶液导致PD和Isc降低到零,其时间过程与不含Cl-的溶液相同。电导率也下降了50%以上。Isc = JCLs导致m--在对照([Na+] = 105 mM)和无Na+条件下,JCLm导致δ = JClnet。当[Na+] = 50 mM(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+](胆碱替代)的依赖性呈S形,表明Na+激活Cl-分泌可能有两个位点。不同[Na+]的1/Isc与1/[Cl-]的图表明,Cl-“载体”的亲和力可能受[Na+]的影响。刺激组织:无Na+(胆碱替代)溶液导致PD、Isc和JClnet均降低至零,但有时含Na+粘膜溶液导致JH增加至对照的50%,而Isc仅增加16%。无Na+的作用不逆转1 mM二丁酰cAMP加0.1 mM异丁基甲基黄嘌呤的serovine解决方案。随着[Na+]的增加,Isc(S形)和JH(单调)均增加。K+取代Na+造成了更大的降低Isc比胆碱时使用; JH保持不变,如果[Na+]大于或等于毫米。我们已经提出,能量依赖的步骤,积极的Cl-运输发生在serenum膜中的Na+-耦合过程。在开路条件下伴随JH的Cl-可以使用单独的系统。
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.