Na/H exchange-dependent cell volume and pH regulation and disturbances.
Na/H exchange-dependent cell volume and pH regulation and disturbances.
复制标题
Na/H 交换依赖的细胞体积和 pH 调节和干扰。
DOI：
10.1016/0300-9629(88)90666-4
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
CragoeJr,EJ
中科院分区：
文献类型：
--
作者：
Cala,PM;Anderson,SE;CragoeJr,EJ
1. 讨论了Na/H交换在细胞体积和pH调节中的作用。此外，还评估了Cl/HCO3交换和系统缓冲液的作用，因为它们与细胞盐和水含量以及细胞内ph的Na/H交换依赖性变化有关。从Amphiuma红细胞研究中获得的数据表明，除了先前报道的Na/H交换依赖的体积调节外，该途径还参与调节细胞ph。这些数据表明，与体积激活的Na/H交换相反，当该途径被pH激活时，它不会作为细胞体积的函数而失活。4. 鉴于Na/H交换的体积和pH调节功能似乎是相互排斥的，我们假设该途径可能在缺氧细胞肿胀（细胞毒性水肿）中发挥作用。5. 在使用23Na核磁共振对灌注兔心脏进行的研究中，我们能够观察到，当钠-钾泵被瓦巴因和/或无钾灌注物抑制时，相对于常氧对照，缺氧心脏的细胞内钠含量增加了5倍。6. 这些研究使我们得出结论，缺氧诱导的钠摄取是由于向内钠泄漏增加而不是钠泵送减少的结果。7. 基于对各种耗散性钠转运抑制剂的研究，我们得出结论，缺氧心脏内钠泄漏的增加是通过Na/H交换。
1. The role of Na/H exchange in cell volume and pH regulation is discussed. In addition the roles of Cl/HCO3 exchange and system buffers are evaluated as they relate to Na/H exchange-dependent changes in cell salt and water content and intracellular pH. 2. Data obtained from studies of Amphiuma red blood cells showed that in addition to previously reported Na/H exchange dependent volume regulation the pathway is also involved in regulating cell pH. 3. These data showed that in contrast to volume activated Na/H exchange, when the pathway is pH activated it does not deactivate as a function of cell volume. 4. Given what appeared to be mutually exclusive volume and pH regulatory functions of the Na/H exchange, we hypothesized that the pathway might play a role in hypoxic cell swelling (cytotoxic edema). 5. In studies performed on perfused rabbit hearts employing 23Na NMR we were able to observe that relative to normoxic controls hypoxic hearts exhibited a five-fold increase in intracellular Na content when the Na-K pump was inhibited by ouabain and/or K-free perfusate. 6. These studies lead us to conclude that hypoxia-induced Na uptake is the result of an increased inward Na leak as opposed to decreased Na pumping. 7. Based upon studies with a variety of inhibitors of dissipative Na transport, we conclude that the increased inward Na leak in hypoxic hearts is via Na/H exchange.