在高渗性收缩过程中，美西螈胃表面上皮细胞的细胞容积调节由钠钾ATP酶和钠钾氯共转运体介导。

Cell volume regulation during hyperosmotic shrinkage is mediated by Na+/K+-ATPase and Na+-K+-2Cl- cotransporter in Necturus gastrics surface epithelial cells.

作者信息

Nylander-Koski Outi, Mustonen Harri, Kiviluoto Tuula, Kivilaakso Eero

机构信息

Department of Surgery, Helsinki University Central Hospital, Biomedicum Helsinki, Haartmaninkatu 8, 00290, Helsinki, Finland.

出版信息

Dig Dis Sci. 2005 Nov;50(11):2043-9. doi: 10.1007/s10620-005-3005-y.

DOI:10.1007/s10620-005-3005-y

PMID:16240213

Abstract

Cell volume regulation was investigated in gastric surface epithelial cells during hypertonic conditions. Isolated Necturus antral mucosa was perfused on the serosal side with Ringer's solution (pH 7.25, 95%O2/5%CO2) and on the mucosal side successively with 150-500 mM NaCl. Amiloride, ouabain, and bumetanide were used to experimentally inhibit Na+/H+, Na+/K+ ATPase or Na+-K+-2Cl- ion transporters. Intracellular sodium activity and cell volume changes were measured with liquid sensor microelectrodes. The increase in intracellular sodium activity caused by luminal hyperosmolar exposure was mainly due to cell shrinkage. Inhibition of Na+/K+ ATPase or Na+-K+-2Cl- cotransporter increased hyperosmotic cell shrinkage (-52 +/- 5%, -85 +/- 19%, and -77 +/- 9% for control, ouabain, and bumetanide, respectively). Inhibition of Na+/K+ ATPase increased intracellular sodium activity (from 18 +/- 4 to 52 +/- 12 mM). Cell volume regulation in gastric epithelial surface cells during mucosal hyperosmolar exposure is maintained by the basolateral Na+-K+-2Cl- cotransporter, while Na+/K+ ATPase maintains sodium balance, but Na+/H+ antiport seems to have a less important role.

摘要

在高渗条件下研究了胃表面上皮细胞的细胞容积调节。将分离的美西螈胃窦黏膜的浆膜侧用林格氏液（pH 7.25，95%O₂/5%CO₂）灌注，黏膜侧依次用150 - 500 mM NaCl灌注。用氨氯吡咪、哇巴因和布美他尼实验性抑制Na⁺/H⁺、Na⁺/K⁺ ATP酶或Na⁺-K⁺-2Cl⁻离子转运体。用液体传感器微电极测量细胞内钠活性和细胞容积变化。管腔高渗暴露引起的细胞内钠活性增加主要是由于细胞收缩。抑制Na⁺/K⁺ ATP酶或Na⁺-K⁺-2Cl⁻共转运体增加了高渗性细胞收缩（对照组、哇巴因组和布美他尼组分别为-52±5%、-85±19%和-77±9%）。抑制Na⁺/K⁺ ATP酶增加了细胞内钠活性（从18±4 mM增至52±12 mM）。黏膜高渗暴露期间胃上皮表面细胞的细胞容积调节由基底外侧Na⁺-K⁺-2Cl⁻共转运体维持，而Na⁺/K⁺ ATP酶维持钠平衡，但Na⁺/H⁺逆向转运似乎作用较小。