Ouabain induces secretion of proatrial natriuretic factor by rat atrial cardiocytes.
Ouabain induces secretion of proatrial natriuretic factor by rat atrial cardiocytes.
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哇巴因诱导大鼠心房心肌细胞分泌心房钠尿因子。
DOI：
10.1152/ajpendo.1988.255.3.e383
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Seidman,JG
中科院分区：
文献类型：
--
作者：
Bloch,KD;Zamir,N;Lichtstein,D;Seidman,CE;Seidman,JG
原代培养的新生大鼠心房和心室心肌细胞分泌心房钠尿因子原 (proANF)，即心房钠尿因子 (ANF) 的 126 个氨基酸前体。两种细胞类型中 proANF 分泌的细胞机制不同：心房心肌细胞在分泌前将 proANF 储存在丰富的分泌颗粒中，而心室心肌细胞在合成后迅速分泌前体。在本研究中，我们使用 Na+-K+-腺苷三磷酸酶 (ATPase) 抑制剂哇巴因来研究这些不同分泌机制的功能意义。哇巴因使心房心肌细胞的免疫反应性 ANF (iANF) 分泌增加 1.5 至 2.4 倍。代谢标记研究表明，proANF 是响应哇巴因释放的 iANF 形式。 iANF 的心室分泌不受 Na+-K+-ATPase 抑制剂的影响。这些观察结果与心房心肌细胞能够通过调节的分泌途径释放 proANF 的模型一致，而心室心肌细胞利用组成型分泌途径。哇巴因刺激 proANF 分泌的能力表明细胞内钙浓度的增加可能促进分泌颗粒与心房细胞膜的融合，从而介导储存的 proANF 的胞吐作用。
Neonatal rat atrial and ventricular cardiocytes in primary culture secrete proatrial natriuretic factor (proANF), the 126-amino acid precursor of atrial natriuretic factor (ANF). The cellular mechanisms of proANF secretion differ in the two cell types: atrial cardiocytes store proANF in abundant secretory granules before secretion, whereas ventricular cardiocytes secrete the precursor rapidly after synthesis. In this study, we used the Na+-K+-adenosinetriphosphatase (ATPase) inhibitor ouabain to investigate the functional significance of these differing secretory mechanisms. Ouabain increased immunoreactive ANF (iANF) secretion by atrial cardiocytes 1.5- to 2.4-fold. Metabolic labeling studies demonstrated that proANF was the form of iANF released in response to ouabain. Ventricular secretion of iANF was unaffected by the Na+-K+-ATPase inhibitor. These observations are consistent with a model in which atrial cardiocytes are able to release proANF via a regulated secretory pathway, whereas ventricular cardiocytes utilize a constitutive secretory pathway. The ability of ouabain to stimulate proANF secretion suggests that an increase in intracellular calcium concentration may promote fusion of secretory granules with atrial cell membranes thereby mediating exocytosis of stored proANF.