Cl- fluxes related to fluid secretion by the rat parotid: involvement of Cl(-)-HCO3- exchange.
Cl- fluxes related to fluid secretion by the rat parotid: involvement of Cl(-)-HCO3- exchange.
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Cl- 通量与大鼠腮腺液体分泌相关：Cl(-)-HCO3- 交换的参与。
DOI：
10.1152/ajpgi.1992.262.3.g393
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Turner,RJ
中科院分区：
文献类型：
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作者：
Melvin,JE;Turner,RJ
在大鼠腮腺腺泡中研究了毒蕈碱诱导的 36Cl- 和 86Rb+（K+ 替代物）通量。刺激导致 Cl- 和 Rb+ 含量快速[半衰期 (t1/2) 小于 30 秒]下降（分别约 50% 和 30%），随后部分恢复较慢（t1/2 约 3-4 分钟）至两种离子静息水平的约 80%。 Cl- 损失可被五纹蝾螈的毒液抑制，该毒液含有 maxi-K+ 通道阻断剂 Charybdotoxin。在布美他尼（一种 Na(+)-K(+)-Cl- 共转运抑制剂）或 HCO3- 去除存在下，Cl- 恢复受到削弱；而在布美他尼和 4,4' 二异硫氰芪-2,2' 二磺酸 (DIDS)（一种 Cl(-)-HCO3- 交换抑制剂）存在下，Cl- 恢复被完全阻断。在含有 HCO3(-) 的培养基中，在转换至无 Cl(-) 溶液的腺泡中观察到快速（t1/2 小于 1 分钟）、DIDS 抑制的细胞质碱化（大约 0.4 pH 单位）。这种碱化在不含 HCO3(-) 的培养基中未见，但在不存在 Na+ 的情况下持续存在，这与存在有效的不依赖 Na(+) 的 Cl(-)-HCO3- 交换剂一致。动力学研究表明，该交换器对细胞外 Cl- 的半最大效应约为 18 mM。这些结果与以下假设一致：唾液腺泡细胞促分泌剂诱导的 KCl 损失是通过电耦合的 K+ 和 Cl- 通道发生的。此外，他们提供了强有力的证据表明，Cl- 进入这些细胞并因此分泌液体是由 Cl(-)-HCO3- 交换和 Na(+)-K(+)-Cl- 共转运介导的。
Muscarinic-induced 36Cl- and 86Rb+ (K+ substitute) fluxes were studied in rat parotid acini. Stimulation resulted in a rapid [half time (t1/2) less than 30 s] decrease in both Cl- and Rb+ content (approximately 50 and 30%, respectively) followed by a slower partial recovery (t1/2 approximately 3-4 min) to approximately 80% of resting levels for both ions. Cl- loss was inhibited by the venom of Leiurus quinquestriatus, which contains the maxi-K+ channel blocker charybdotoxin. Cl- recovery was blunted in the presence of bumetanide, an inhibitor of Na(+)-K(+)-Cl- cotransport, or on HCO3- removal and was completely blocked in the presence of bumetanide and 4,4' diisothiocyanostilbene-2,2' disulfonic acid (DIDS), an inhibitor of Cl(-)-HCO3- exchange. In HCO3(-)-containing medium a rapid (t1/2 less than 1 min), DIDS-inhibitable cytoplasmic alkalinization (approximately 0.4 pH unit) was observed in acini switched to a Cl(-)-free solution. This alkalinization was not seen in HCO3(-)-free medium but persisted in the absence of Na+, consistent with the presence of a potent Na(+)-independent Cl(-)-HCO3- exchanger. Kinetic studies indicated that the half-maximal effect of this exchanger for extracellular Cl- was approximately 18 mM. These results are consistent with the hypothesis that secretagogue-induced KCl loss by salivary acinar cells occurs via electrically coupled K+ and Cl- channels. In addition, they provide strong evidence that Cl- entry into, and thus fluid secretion by, these cells is mediated by both Cl(-)-HCO3- exchange and Na(+)-K(+)-Cl- cotransport.