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首页> 外文期刊>American Journal of Physiology >Mechanisms of secretion-associated shrinkage and volume recovery in cultured rabbit parietal cells.
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Mechanisms of secretion-associated shrinkage and volume recovery in cultured rabbit parietal cells.

机译：在培养的兔壁细胞中分泌相关的收缩和体积恢复的机制。

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摘要

We have previously shown that stimulation of acid secretion in parietal cells causes rapid initial cell shrinkage, followed by Na(+)/H(+) exchange-mediated regulatory volume increase (RVI). The factors leading to the initial cell shrinkage are unknown. We therefore monitored volume changes in cultured rabbit parietal cells by confocal measurement of the cytoplasmic calcein concentration. Although blocking the presumably apically located K(+) channel KCNQ1 with chromanol 293b reduced both the forskolin- and carbachol-induced cell shrinkage, inhibition of Ca(2+)-sensitive K(+) channels with charybdotoxin strongly inhibited the cell volume decrease after carbachol, but not after forskolin stimulation. The cell shrinkage induced by both secretagogues was partially inhibited by blocking H(+)-K(+)-ATPase with SCH28080 and completely absent after incubation with NPPB, which inhibits parietal cell anion conductances involved in acid secretion. The subsequent RVI was strongly inhibited with the Na(+)/H(+) exchanger 1 (NHE1)-specific concentration of HOE642 and completely by 500 muM dimethyl-amiloride (DMA), which also inhibits NHE4. None of the above substances induced volume changes under baseline conditions. Our results indicate that cell volume decrease associated with acid secretion is dependent on the activation of K(+) and Cl(-) channels by the respective secretagogues. K(+), Cl(-), and water secretion into the secretory canaliculi is thus one likely mechanism of stimulation-associated cell shrinkage in cultured parietal cells. The observed RVI is predominantly mediated by NHE1.
机译：我们以前已经表明刺激壁细胞中的酸分泌会引起细胞初始快速收缩，然后是Na（+）/ H（+）交换介导的调节体积增加（RVI）。导致初始细胞收缩的因素尚不清楚。因此，我们通过共聚焦测量胞质钙黄绿素浓度来监测培养的兔壁细胞的体积变化。尽管用苯并二氢苯并二氢吡喃-2-甲基-2-苯并咪唑293b阻断了可能位于顶端的K（+）通道KCNQ1减少了福司可林和卡巴胆碱诱导的细胞收缩，但是抑制Ca（2+）敏感的K（+）通道具有charybdotoxin强烈抑制了细胞体积的减少。卡巴胆碱，但在福斯高林刺激后不起作用。两种促泌剂诱导的细胞收缩均被SCH28080阻断H（+）-K（+）-ATPase所部分抑制，与NPPB孵育后则完全不存在，从而抑制了参与酸分泌的壁细胞阴离子电导。后续的RVI被Na（+）/ H（+）交换剂1（NHE1）特异性浓度的HOE642强烈抑制，并完全被500μM的二甲基阿米洛利（DMA）抑制，后者也抑制了NHE4。在基线条件下，以上物质均未引起体积变化。我们的结果表明，与酸分泌有关的细胞体积减少取决于各个促分泌素对K（+）和Cl（-）通道的激活。因此，K（+），Cl（-）和水分泌到分泌小管中是刺激的壁细胞刺激相关细胞收缩的一种可能机制。观察到的RVI主要由NHE1介导。

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