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首页> 外文期刊>Journal of Comparative Physiology, B. Biochemical, Systemic, and Environmental Physiology >Ca++ regulation of paracellular permeability in the middle intestine ofthe eel, Anguilla anguilla
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Ca++ regulation of paracellular permeability in the middle intestine ofthe eel, Anguilla anguilla

机译：Ca ++调节鳗gu中肠细胞旁通透性

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摘要

The role of Ca++ on the regulation of the paracellular pathway permeability of the middle intestine of Anguilla anguilla was studied by measuring the transepithelial resistance and the dilution potential, generated when one half of NaCl in the mucosal solution was substituted iso-osmotically with mannitol, in various experimental conditions altering extracellular and/or intracellular calcium levels. We found that removal of Ca++ in the presence of ethylene glycol-bis(beta -amino-ethyl ether) (EGTA) from both the mucosal and the serosal side, but not from one side only, reduced both the transepithelial resistance and the magnitude of the dilution potential. The irreversibility of this effect suggests a destruction of the organization of the junction in the nominal absence of Ca++. However a modulatory role of extracellular Ca++ cannot be excluded. The decrease of the intracellular Ca++ activity. produced by using verapamil to block the Ca++ entry into the cell, or by adding 3,4,5-trimethoxybenzoic acid 8-(diethylamino) octyl ester (hydrochloride) (TMB-8), an inhibitor of Ca++ release from the intracellular stores, reduced both the transepithelial resistance and the magnitude of the dilution potential, indicating a role of cytosolic Ca++ in the modulation of the paracellular permeability. However the rise of calcium activity produced by the Ca++ ionophore calcimycin (A23187) evoked an identical effect, suggesting that any change in physiological intracellular Ca++ activity alters the paracellular permeability.
机译：通过测量粘膜溶液中一半的NaCl被甘露醇等渗取代后产生的跨上皮抵抗力和稀释电位，研究了Ca ++在调节安圭拉中肠小肠旁通路通透性中的作用。改变细胞外和/或细胞内钙水平的各种实验条件。我们发现，在存在乙二醇-双（β-氨基-乙基醚）（EGTA）的情况下，从粘膜和浆膜侧（而不是仅从一侧）去除Ca ++会降低跨上皮的抵抗力并降低稀释潜力。这种作用的不可逆性表明，在名义上不存在Ca ++的情况下，会破坏连接的组织。但是，不能排除细胞外Ca ++的调节作用。细胞内Ca ++活性的降低。通过使用维拉帕米来阻止Ca ++进入细胞或通过添加3,4,5-三甲氧基苯甲酸8-（二乙基氨基）辛基酯（盐酸盐）（TMB-8）产生的，Ca ++是从细胞内存储释放的抑制剂，降低了跨上皮的抵抗力和稀释电位的幅度，表明胞质Ca ++在调节旁细胞通透性中的作用。然而，由Ca ++离子载体钙霉素（A23187）产生的钙活性的升高引起了相同的作用，表明生理细胞内Ca ++活性的任何变化都会改变细胞旁的通透性。

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