首页> 美国卫生研究院文献>British Journal of Pharmacology and Chemotherapy >Effects of noradrenaline vasopressin and angiotensin on the Na-K pump in rat isolated liver cells.
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Effects of noradrenaline vasopressin and angiotensin on the Na-K pump in rat isolated liver cells.

机译:去甲肾上腺素血管加压素和血管紧张素对大鼠离体肝细胞Na-K泵的影响。

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摘要

The effects of noradenaline (via alpha 1-adrenoceptors) and of the peptidic hormones vasopressin and angiotensin on the Na-K pump have been studied in rat isolated liver cells. The three hormones increased the cytosolic Ca concentration, stimulated the Na-K pump and decreased the internal Na concentration of the cells. The effects were dose-dependent and were blocked by the corresponding antagonists. The simultaneous addition of maximal doses of noradrenaline and angiotensin or vasopressin were not additive suggesting that the hormones use a common mechanism to stimulate the carrier. Incubating the cells in Ca-free medium for long periods (Ca-depletion) increased the Na-K pump activity and reduced the stimulatory action of vasopressin, angiotensin and noradrenaline. The effect of the Ca indicator quin2, used as an intracellular Ca chelator, was also studied. The cells were loaded with a maximal concentration of [3H]-quin2 acetoxymethyl ester in the presence of external Ca for 6 min. The final cell content was 3.1 nmol quin2 mg-1 cell dry wt. In these cells the cytosolic Ca, as monitored from the fluorescence emission of the indicator, was about 200 nM and Na-K pump activity was normal and the cells remained responsive to the three hormones. Loading the cells with quin2 in the absence of external Ca reduced the [Ca]i from 200 nM to about 40 nM and increased the Na-K pump activity but not as a result of a rise in internal Na concentration. In addition, the rat hepatocytes were no longer sensitive to the hormones. It is proposed that Ca inhibits the Na-K pump by binding the internal sites and that vasopressin, angiotensin and noradrenaline stimulate the carrier by interfering with the inhibitory Ca sites.
机译:已经在大鼠分离的肝细胞中研究了去甲肾上腺素(通过α1-肾上腺素受体)以及肽激素血管加压素和血管紧张素对Na-K泵的作用。这三种激素增加了细胞内Ca的浓度,刺激了Na-K泵并降低了细胞内部的Na浓度。作用是剂量依赖性的,并被相应的拮抗剂阻断。同时添加最大剂量的去甲肾上腺素和血管紧张素或加压素并没有累加,这表明激素使用共同的机制刺激载体。在无钙培养基中长期培养细胞(消除钙)可增加Na-K泵的活性,并降低血管加压素,血管紧张素和去甲肾上腺素的刺激作用。还研究了用作细胞内钙螯合剂的钙指示剂quin2的作用。在外部Ca存在下,将最大浓度的[3H] -quin2乙酰氧基甲基酯加载到细胞中6分钟。最终细胞含量为3.1 nmol quin2 mg-1细胞干重。在这些细胞中,从指示剂的荧光发射监测到的胞质Ca约为200 nM,Na-K泵浦活性正常,细胞仍然对这三种激素有反应。在不存在外部Ca的情况下用quin2加载细胞,将[Ca] i从200 nM降低至约40 nM,并增加了Na-K泵浦活性,但这不是内部Na浓度升高的结果。另外,大鼠肝细胞对激素不再敏感。提出Ca通过结合内部位点抑制Na-K泵,而血管加压素,血管紧张素和去甲肾上腺素通过干扰抑制性Ca位点来刺激载体。

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