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首页> 外文期刊>Life sciences >Ouabain stimulates atrial natriuretic peptide secretion via the endothelin-1/ET B receptor-mediated pathway in beating rabbit atria
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Ouabain stimulates atrial natriuretic peptide secretion via the endothelin-1/ET B receptor-mediated pathway in beating rabbit atria

机译：哇巴因通过跳动的兔心房中内皮素-1 / ET B受体介导的途径刺激心钠素分泌

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Aims: Ouabain has been reported to increase the secretion of atrial natriuretic peptide (ANP) in vitro. However, the mechanism by which ouabain increases ANP secretion is not well known. Therefore, the purpose of the present study was to investigate the underlying mechanism of ouabain-stimulated ANP secretion. Main methods: A perfused beating rabbit atrial model was used. The ANP and ET-1 levels in the atrial perfusates were measured by radioimmunoassays. Key findings: Ouabain (1.0, 3.0 and 6.0 μmol/L) significantly increased atrial ANP secretion in a dose-dependent manner, while the endothelin (ET)-1 levels were increased by the higher doses (3.0 and 6.0 μmol/L) of ouabain. Ouabain-increased atrial ET-1 release was blocked by PD98059 (30.0 μmol/L), an inhibitor of mitogen-activated protein kinase (MAPK). Nifedipine (1.0 μmol/L), an inhibitor of L-type Ca 2+ channels, completely abolished ouabain-increased ANP secretion without changing the ouabain-induced atrial dynamics. KB-R7943 (3.0 μmol/L), an inhibitor of Na +-Ca 2+ exchangers, completely blocked the effects of ouabain-increased atrial dynamics, but did not modulate ouabain-increased ANP secretion. ET-1 significantly stimulated atrial ANP release in a dose-dependent manner. The effects of ET-1 and ouabain on ANP secretion were completely blocked by BQ788 (0.3 μmol/L), an inhibitor of ET-1 type B (ET B) receptors, but not by BQ123 (0.3 μM), an inhibitor of ET-1 type A receptors. Ouabain-increased atrial ANP secretion was blocked by PD98059 and indomethacin (30.0 μmol/L), an inhibitor of cyclooxygenase. Significance: Ouabain significantly stimulated atrial ANP secretion via an ET-1-ET B receptor-mediated pathway involving MAPK signaling pathway activation and prostaglandin formation.
机译：目的：据报道，瓦巴因在体外可增加心钠素的分泌。但是，哇巴因增加ANP分泌的机制尚不清楚。因此，本研究的目的是研究哇巴因刺激的ANP分泌的潜在机制。主要方法：使用灌注的跳动兔心房模型。通过放射免疫测定法测量心房灌注液中的ANP和ET-1水平。主要发现：哇巴因（1.0、3.0和6.0μmol/ L）以剂量依赖性方式显着增加心房ANP的分泌，而较高剂量（3.0和6.0μmol/ L）的内皮素（ET）-1水平增加哇巴因经由增丝分裂原活化蛋白激酶（MAPK）抑制剂PD98059（30.0μmol/ L）阻止了哇巴因增加的心房ET-1释放。硝苯地平（1.0μmol/ L）是L型Ca 2+通道的抑制剂，完全消除了哇巴因增加的ANP分泌，而没有改变哇巴因引起的心房动力学。 Na + -Ca 2+交换剂的抑制剂KB-R7943（3.0μmol/ L）完全阻断了哇巴因增加心房动力学的作用，但没有调节哇巴因增加的ANP分泌。 ET-1以剂量依赖性方式显着刺激心房ANP释放。 ET-1 B（ET B）受体的抑制剂BQ788（0.3μmol/ L）完全阻断了ET-1和哇巴因对ANP分泌的影响，但并未被ET抑制剂BQ123（0.3μM）完全阻断-1型A受体。 PD98059和环氧合酶抑制剂吲哚美辛（30.0μmol/ L）阻止了哇巴因增加的心房ANP分泌。意义：哇巴因通过ET-1-ET B受体介导的途径（包括MAPK信号通路激活和前列腺素形成）显着刺激心房ANP分泌。

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