蛋白激酶C参与血管紧张素ii介导的牛肾上腺肾小球细胞中12-羟基二十碳四烯酸的释放。

H Shibata, I Kojima
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引用次数: 5

摘要

本研究旨在确定蛋白激酶C是否参与血管紧张素ii介导的牛肾上腺肾小球细胞中12-羟基二碳四烯酸(12-HETE)的释放。蛋白激酶C的激活剂,12- o -十四烷醇- 4-乙酸酯(TPA)和1-油基-2-乙酰甘油(OAG),显著增加12-HETE的释放。钙离子进入刺激剂BAYK8644可增强OAG的作用。体外抑制蛋白激酶C活性的鞘氨醇、H-7和星孢素几乎完全阻断TPA诱导的12-HETE释放。这些药物也显著降低血管紧张素ii介导的12-HETE释放。测量12-HETE释放的时间过程,血管紧张素II引起12-HETE的缓释,而staurosporine抑制了这种缓释。这些结果表明,血管紧张素II诱导了醛固酮分泌前传调节剂12-HETE的持续释放,蛋白激酶C可能参与了这一过程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Involvement of protein kinase C in angiotensin II-mediated release of 12-hydroxyeicosatetraenoic acid in bovine adrenal glomerulosa cells.

The present study was conducted to determine whether protein kinase C was involved in angiotensin II-mediated release of 12-hydroxyeicosatetraenoic acid (12-HETE) from bovine adrenal glomerulosa cells. Activators of protein kinase C, 12-O-tetradecanoylphorbol 4-acetate (TPA) and 1-oleoyl-2-acetylglycerol (OAG), significantly increased release of 12-HETE. The effect of OAG was potentiated by BAYK8644, a stimulator of calcium entry. Sphingosine, H-7 and staurosporine, which inhibited the activity of protein kinase C in vitro, almost completely blocked 12-HETE release induced by TPA. These agents also significantly reduced angiotensin II-mediated 12-HETE release. When time course of the liberation of 12-HETE was measured, angiotensin II elicited sustained release of 12-HETE, which was inhibited by staurosporine. These results indicate that angiotensin II induces sustained release of 12-HETE, a feed forward regulator of aldosterone secretion, and that protein kinase C may be involved in this process.

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