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Hypertonicity-induced intracellular pH changes in rat mast cells

机译：高渗引起的大鼠肥大细胞内pH变化

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摘要

In a non-isotonic environment, cells can shrink or swell and return to their normal shape by activating ion transport pathways. Changes in intracellular pH (pHi) after osmotic stress have been identified in several cells. In order to study the mechanisms that regulate cytosolic pH of rat mast cells in a hypertonic medium, we used the pH sensitive dye, BCECF. Under these hypertonic conditions, pHi undergoes an alkalinization following an initial acidification. The alkalinization is mediated by a Na+/H+ exchanger, since it is inhibited by amiloride and lack of extracellular sodium. Under these conditions, the alkalinization is increased with the PKC activators, TPA and GAG, and partially blocked with trifluoperazine, an unspecific protein kinase C (PKC) and Ca+2 calmodulin-dependent protein kinases (Ca+2/CaM Ii) inhibitor. There is also an anion exchanger, blocked with DIDS but not activated by PKC, that participates in the observed alkalinization. However, Na+/M+ exchanger is the main mechanism involved in the alkalinization of pHi of mast cells in a hyperosmotic environment. (C) 2000 Elsevier Science Inc. All rights reserved. [References: 50]
机译：在非等渗环境中，细胞可以通过激活离子传输途径而收缩或膨胀并恢复其正常形状。渗透应激后细胞内pH（pHi）的变化已在几个细胞中被确定。为了研究在高渗介质中调节大鼠肥大细胞胞质pH的机制，我们使用了pH敏感染料BCECF。在这些高渗条件下，pHi在初始酸化之后经历碱化。碱化作用是由Na + / H +交换剂介导的，因为它受到阿米洛利和缺乏细胞外钠的抑制。在这些条件下，通过PKC活化剂，TPA和GAG可以增加碱化作用，并被三氟拉嗪，一种非特异性蛋白激酶C（PKC）和钙+钙调蛋白依赖性蛋白激酶（Ca + 2 / CaM Ii）抑制剂部分阻断。还有一个阴离子交换剂，被DIDS阻滞但未被PKC活化，它参与观察到的碱化反应。然而，在高渗环境中，Na + / M +交换子是肥大细胞pHi碱化的主要机制。 （C）2000 Elsevier Science Inc.保留所有权利。 [参考：50]

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