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首页> 外文期刊>Cellular Physiology and Biochemistry >beta(2)-Adrenergic Stimulation Blunts Inhibition of Epithelial Ion Transport by Hypoxia of Rat Alveolar Epithelial Cells
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beta(2)-Adrenergic Stimulation Blunts Inhibition of Epithelial Ion Transport by Hypoxia of Rat Alveolar Epithelial Cells

机译：β（2）-肾上腺素刺激钝化大鼠肺泡上皮细胞缺氧对上皮离子运输的抑制作用

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Hypoxia impairs alveolar fluid clearance by inhibition of Na+ reabsorption, and also impairs beta(2) adrenergic signaling in alveolar epithelium. Since both are major rescue mechanisms preventing pulmonary edema, we studied whether acute and prolonged treatment with terbutaline would prevent hypoxic inhibition of ion transport. Short circuit currents (ISC) were measured on normoxic and hypoxic (1.5% O-2; 24h) primary rat alveolar type II (ATII) cells in absence and presence of terbutaline (1 to 100 mu M, 24h). Control and pre-treated cells were stimulated acutely with terbutaline. Transepithelial transport was measured as short circuit current (ISC) in Ussing chambers. Terbutaline induced a rapid decrease ISC (-20%) followed by a slow raise. The transient change in ISC was not inhibited by amiloride but was prevented after Cl- depletion indicating a Cl- current. The slow increase after this transient was amiloride-sensitive indicating a Na+ current. Total ISC, its amiloride-sensitive component, and the transient decrease upon terbutaline stimulation were decreased by hypoxia. 24h treatment with terbutaline stimulated these currents in normoxia and hypoxia, although stimulation was less in the latter. 24h treatment with terbutaline increased the capacity of Na+/K+-ATPase and ENaC as measured after permeabilization with amphotericin. These changes were not paralleled by altered mRNA expression. Acutely applied terbutaline induced a 4-fold increase in cAMP formation in normoxia; terbutaline-induced cAMP-formation was impaired by hypoxia (-20%). Pre-treatment with terbutaline for 24h decreased terbutaline-induced cAMP formation by 85%. Despite this desensitization, addition of terbutaline to terbutaline pre-treated cells caused a larger increase in Cl- and Na+ transport both in normoxia and hypoxia than in non pre-treated cells. These results indicate that beta(2) adrenergic stimulation increased Na+- and Cl- transport in ATII cells even in hypoxia thus restoring normal reabsorption.
机译：缺氧通过抑制Na +重吸收来损害肺泡液清除，并损害肺泡上皮中的β（2）肾上腺素信号传导。由于两者都是预防肺水肿的主要救护机制，因此我们研究了特布他林的急性和长期治疗是否可以防止低氧抑制离子转运。在缺乏和存在特布他林的情况下（1至100μM，24h），对常氧和低氧（1.5％O-2; 24h）原代大鼠II型肺泡（ATII）细胞进行短路电流（ISC）测量。用特布他林急性刺激对照细胞和预处理细胞。经上皮运输测量为在Usssing室的短路电流（ISC）。特布他林引起ISC迅速下降（-20％），然后缓慢上升。 ISC的瞬态变化不受阿米洛利抑制，但在Cl-耗尽（指示Cl-电流）后被阻止。此瞬变后的缓慢增加对阿米洛利敏感，表明存在Na +电流。总ISC，其对阿米洛利敏感的成分以及特布他林刺激后的短暂减少因缺氧而减少。特布他林24小时治疗在常氧和低氧时刺激了这些电流，尽管后者的刺激较少。用两性霉素透化后，特布他林处理24h可增加Na + / K + -ATPase和ENaC的能力。这些改变与改变的mRNA表达没有平行。急性应用特布他林可在常氧中诱导cAMP形成增加4倍;缺氧会损害特布他林诱导的cAMP的形成（-20％）。特布他林预处理24小时可将特布他林诱导的cAMP形成减少85％。尽管有这种脱敏作用，但在常氧和低氧条件下，将特布他林添加到特布他林预处理的细胞中会导致Cl-和Na +转运的增加大于未预处理的细胞。这些结果表明，即使在缺氧状态下，β（2）肾上腺素刺激也会增加ATII细胞中的Na +和Cl-转运，从而恢复正常的重吸收。

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