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首页> 外文期刊>Cellular Physiology and Biochemistry >Mechanisms of Isoform-Specific Na/K Pump Regulation by Short- and Long-Term Adrenergic Activation in Rat Ventricular Myocytes
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Mechanisms of Isoform-Specific Na/K Pump Regulation by Short- and Long-Term Adrenergic Activation in Rat Ventricular Myocytes

机译：短期和长期肾上腺素能激活大鼠心室肌细胞的亚型特定Na / K泵调节机制。

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biBackground /i/bMany stressful conditions, including cardiovascular diseases, induce long-term elevations in circulating catecholamines, thereby leading to changes of the Na/K pump and thus affecting myocardial functions. However, only short-term adrenergic regulation of the Na/K pump has been reported. The present study is the first investigation of long-term adrenergic regulation of the Na/K pump and the potential mechanism. biMethods /i/bAfter acutely isolated Sprague-Dawley rat myocytes were incubated with noradrenaline or isoprenaline for 24 h, Na/K pump high- (IsubPH/sub) and low-affinity current (IsubPL/sub), α-isoform mRNA, and α-isoform protein were examined using patch-clamp, RT-PCR, and Western blotting techniques, respectively. biResults /i/bAfter the short-term incubation, isoprenaline reduced the IsubPL/sub through a PKA-dependent pathway that involves αsub1/sub-isoform translocation from the membrane to early endosomes, and noradrenaline increased the IsubPH/sub through a PKC-dependent pathway that involves αsub2/sub-isoform translocation from late endosomes to the membrane. After long-term incubation, isoprenaline increased the IsubPL/sub, αsub1/sub-isoform mRNA, and αsub1/sub-isoform protein, and noradrenaline reduced the IsubPH/sub, αsub2/sub-isoform mRNA, and αsub1/sub-isoform protein through a PKA-or PKC-dependent pathway, respectively. biConclusions /i/bThese results suggest that long-term adrenergic Na/K pump regulation is isoform-specific and negatively feeds back on the short-term response. Furthermore, long-term regulation involves transcription and translation of the respective α-isoform, whereas short-term regulation involves the translocation of the available α-isoform to the plasma membrane.
机译：背景 许多压力条件，包括心血管疾病，会导致循环儿茶酚胺的长期升高，从而导致Na / K泵的改变，从而影响心肌功能。然而，仅报道了Na / K泵的短期肾上腺素能调节。本研究是对Na / K泵的长期肾上腺素能调节及其潜在机制的首次研究。 方法 将急性分离的Sprague-Dawley大鼠心肌细胞与去甲肾上腺素或异丙肾上腺素温育24小时后，Na / K泵高（I PH ）分别使用膜片钳，RT-PCR和Western印迹技术检测低亲和电流（I PL ），α-亚型mRNA和α-亚型蛋白。 结果 短期孵育后，异丙肾上腺素通过涉及α 1 PL 从膜到早期内体的>-亚型易位，去甲肾上腺素通过PKC依赖性途径增加I PH ，该途径涉及从晚期内体到膜的α 2 亚型的易位。 。长期孵育后，异丙肾上腺素会增加I PL ，α 1 -亚型mRNA和α 1 -亚型的蛋白，而去甲肾上腺素会降低I PH ，α 2 -异构体mRNA和α 1 -异构体蛋白分别通过PKA或PKC依赖性途径发生。 结论 这些结果表明，长期肾上腺素钠/钾泵调节是特定于异构体的，并且对短期反应产生负面反馈。此外，长期调节涉及各个α同工型的转录和翻译，而短期调节涉及可利用的α同工型向质膜的转运。

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