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首页> 外文期刊>Life sciences >STIMULATION OF RB+ INFLUX BY BRADYKININ THROUGH NA+/K+/CL- COTRANSPORT AND NA+/K+-ATPASE IN NIH-3T3 FIBROBLASTS
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STIMULATION OF RB+ INFLUX BY BRADYKININ THROUGH NA+/K+/CL- COTRANSPORT AND NA+/K+-ATPASE IN NIH-3T3 FIBROBLASTS

机译：缓激肽通过NIH-3T3成纤维细胞中NA + / K + / CL-共转运和NA + / K + -ATPase刺激RB +内流

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Bradykinin receptor stimulation results in G-protein-coupled phospholipase activation, initiating protein kinase C (PKC) stimulation and cytosolic free Ca2+ concentration ([Ca2+](i)) rises as signalling pathways. Using Rbf as a tracer for K+ we have studied the mechanisms involved in bradykinin-stimulated Rb+ influx in NM-3T3 fibroblasts. The furosemide-sensitive Na+/K+/Cl- cotransport and the ouabain-sensitive Na+/K+-ATPase were both involved in Rb+ influx under resting conditions with a ratio Na+/K+/Cl- cotransport / Na+/K+-ATPase (r) = 0.73. Bradykinin stimulated Rb+ influx (+82.6%) through both systems without changing their ratio (r = 0.72). PKC stimulation by a 15-min-treatment with phorbol 12-myristate 13-acetate (PMA) (2x10(-7) M) increased Rbf influx in resting cells by 75.7% without affecting r (0.75). PKC inhibition by H-7, and PKC down-regulation by 24-h PMA (10(-6) M) treatment decreased the bradykinin-induced stimulation of Rb+ influx (+31% and +14.9% above control respectively). Both down-regulation and inhibition of PKC dramatically reduced the furosemide-sensitive Na+/K+/Cl- cotransport, as r fell to 0.239 and 0.032 in bradykinin-stimulated cells after H-7 and 24-h PMA treatments, respectively. BAPTA/AM pretreatment (10(-4) M, 60 min), which complexed with [Ca2+](i), not only prevented the bradykinin-induced [Ca2+](i) raise, but also partially inhibited bradykinin-induced Rb+ influx stimulation (+39% above control), without modifying r (0.76). We conclude that stimulation of PKC is a major pathway involved in bradykinin stimulation of Rb+ influx in NM-3T3 fibroblasts, and that rises in [Ca2+](i) participate in bradykinin signalling, possibly through PKC activation. Our data also suggest that active PKC is required for basal and bradykinin-stimulated Na+/K+/Cl- cotransport activity in these cells. [References: 22]
机译：缓激肽受体的刺激导致G蛋白偶联的磷脂酶激活，引发蛋白激酶C（PKC）刺激和细胞质游离Ca2 +浓度（[Ca2 +]（i））随着信号通路的增加而升高。使用Rbf作为K +的示踪剂，我们研究了缓激肽刺激的NM-3T3成纤维细胞Rb +内流的机制。速尿敏感的Na + / K + / Cl-共转运和哇巴因敏感的Na + / K + -ATPase都在静息条件下参与Rb +的涌入，比例为Na + / K + / Cl-共转运/ Na + / K + -ATPase（r）= 0.73。缓激肽通过两个系统刺激Rb +内流（+ 82.6％），而不会改变它们的比率（r = 0.72）。用佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）（2x10（-7）M）处理15分钟可刺激PKC，使静息细胞Rbf内流增加75.7％，而不会影响r（0.75）。 H-7对PKC的抑制作用以及24小时PMA（10（-6）M）处理对PKC的下调作用降低了缓激肽诱导的Rb +内流刺激（分别比对照高31％和+ 14.9％）。 PKC的下调和抑制都显着降低了速尿敏感的Na + / K + / Cl-共转运，因为在分别接受H-7和24小时PMA处理后，缓激肽刺激的细胞r分别降至0.239和0.032。 BAPTA / AM预处理（10（-4）M，60分钟）与[Ca2 +]（i）络合，不仅防止了缓激肽诱导的[Ca2 +]（i）升高，而且部分抑制了缓激肽诱导的Rb +内流刺激（比对照组高39％），而未修改r（0.76）。我们得出的结论是，PKC的刺激是缓激肽刺激NM-3T3成纤维细胞Rb +内流的主要途径，并且[Ca2 +]（i）的升高可能通过PKC激活参与了缓激肽的信号传导。我们的数据还表明，在这些细胞中，基础和缓激肽刺激的Na + / K + / Cl-共转运活性需要活性PKC。 [参考：22]

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