beta(2)-agonist regulation of cell volume in fetal distal lung epithelium by cAMP-independent Ca2+ release from intracellular stores
beta(2)-agonist regulation of cell volume in fetal distal lung epithelium by cAMP-independent Ca2+ release from intracellular stores
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DOI：
10.1139/cjpp-75-8-1030
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发表时间：
1997-08-01
影响因子：
2.1
通讯作者：
Marunaka, Y
中科院分区：
文献类型：
--
作者：
Niisato, N;Nakahari, T;Marunaka, Y
研究了β(2)-肾上腺素能受体激动剂（β(2)，激动剂）和cAMP对胎儿远端肺上皮细胞胞浆Ca2+浓度（[Ca2+](c)）和细胞体积的影响。特布他林（一种特异性β(2)激动剂，10 μ M）和二丁基cAMP （DBcAMP, 1 mM）在细胞外Ca2+存在下增加[Ca2+](c)。即使在没有细胞外Ca2+的情况下，特布他林诱导的[Ca2+](c)的增加仍然被观察到，尽管增加是短暂的。然而，DBcAMP没有引起[Ca2+]的显著变化(c)。在1 mM细胞外Ca2+存在的情况下，特布他林和DBcAMP诱导奎宁（K+通道阻滞剂）敏感细胞收缩。然而，在无Ca2+溶液中，特布他林诱导细胞快速收缩，其次是苯甲胺（一种特定的Na+通道阻滞剂，类似于阿米洛胺）敏感的短暂细胞肿胀。在无Ca2+溶液中，DBcAMP诱导苯甲酰胺敏感的短暂细胞肿胀而不发生细胞收缩。综上所述，我们的观察表明，β(2)激动剂通过增加细胞外空间的Ca2+内流和细胞内Ca2+储存的Ca2+释放来诱导[Ca2+](c)的升高，而DBcAMP仅刺激细胞外空间的Ca2+内流。此外，特布他林和DBcAMP激活苯甲胺敏感通道独立于[Ca2+]的增加(c)。
The effects of beta(2)-adrenoceptor agonist (beta(2), agonist) and cAMP on cytosolic Ca2+ concentration ([Ca2+](c)) and cell volume were studied in fetal distal lung epithelial cells. Both terbutaline (a specific beta(2) agonist, 10 mu M) and dibutyryl cAMP (DBcAMP, 1 mM) increased [Ca2+](c) in the presence of extracellular Ca2+. Even in the absence of extracellular Ca2+, the terbutaline-induced increase in [Ca2+](c) was still observed, although the increase was transient. However, DBcAMP caused no significant change in [Ca2+](c). In the presence of 1 mM extracellular Ca2+, terbutaline and DBcAMP induced quinine (a blocker of K+ channel) sensitive cell shrinkage. However, in a Ca2+-free solution, terbutaline induced rapid cell shrinkage, followed by benzamil (a specific blocker of Na+ channel, an analogue of amiloride) sensitive transient cell swelling. In a Ca2+-free solution, DBcAMP induced benzamil-sensitive transient cell swelling without cell shrinkage. Taken together, our observations indicate that the beta(2) agonist induced an elevation of [Ca2+](c) by increasing both a Ca2+ influx from the extracellular space and a Ca2+ release from intracellular Ca2+ stores, whereas DBcAMP only stimulated Ca2+ influx from the extracellular space. Furthermore, it is suggested that terbutaline and DBcAMP activated benzamil-sensitive channels independently of an increase in [Ca2+](c).