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首页> 外文期刊>American Journal of Physiology >Adrenal-dependent modulation of the catalytic subunit isoforms of the Na+-K+-ATPase in aorta.
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Adrenal-dependent modulation of the catalytic subunit isoforms of the Na+-K+-ATPase in aorta.

机译:肾上腺依赖的主动脉中Na + -K + -ATPase催化亚基亚型的调节。

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Na+-K+-ATPase gene expression and activity were studied in aortas from adrenalectomized (ADX) rats and ADX rats with deoxycorticosterone supplement (ADX-DOCA). Northern analysis of RNA from ADX rats revealed a significant decrease in alpha2-mRNA levels (38.5 +/- 8.3% of control, P < 0.01) that was prevented by DOCA (P < 0.05). A decrease to 55.8 +/- 7.7% in alpha2-isoform protein was observed 8 days after adrenal removal (P < 0.05); DOCA reversed this effect (90.8 +/- 10.5%). Adrenalectomy induced a decrease of 68.5 +/- 4.5% in beta1-mRNA (P < 0.01) and 52.7 +/- 8.3% in ADX-DOCA rats (P < 0.01). Also, a reduction in beta1-isoform protein that was not prevented by DOCA was detected after adrenalectomy (47.1 +/- 11%, P < 0.01). In contrast, no differences in alpha1-mRNA or -protein levels were observed. Vascular sodium pump activity was reduced to 59.8 +/- 4.6% of control values after adrenalectomy (P < 0.01); this reduction was reversed by DOCA. Our data indicate that corticosteroids regulate Na+-K+-ATPase isoform expression and activity in vascular tissue in vivo, suggesting a mineralocorticoid-dependent modulation of alpha2-Na+-K+-ATPase gene expression in aorta, with beta1-isoform expression dependent on the presence of glucocorticoids.
机译:在肾上腺切除(ADX)大鼠和补充脱氧皮质酮的ADX大鼠(ADX-DOCA)的主动脉中研究了Na + -K + -ATPase基因的表达和活性。对来自ADX大鼠的RNA进行的Northern分析表明,DOCA阻止了α2-mRNA水平的显着降低(对照组的38.5 +/- 8.3%,P <0.01)(P <0.05)。去除肾上腺后8天,α2-同工型蛋白下降到55.8 +/- 7.7%(P <0.05); DOCA扭转了这种影响(90.8 +/- 10.5%)。肾上腺切除术导致beta1-mRNA下降68.5 +/- 4.5%(P <0.01),而ADX-DOCA大鼠下降52.7 +/- 8.3%(P <0.01)。另外,肾上腺切除术后未检测到DOCA未能阻止的β1异构体蛋白的降低(47.1 +/- 11%,P <0.01)。相反,未观察到α1-mRNA或-蛋白水平的差异。肾上腺切除术后血管钠泵活性降至对照值的59.8 +/- 4.6%(P <0.01); DOCA撤消了这种减少。我们的数据表明皮质类固醇调节体内血管组织中的Na + -K + -ATPase同工型表达和活性,这表明主动脉中α2-Na+ -K + -ATPase基因表达的盐皮质激素依赖性调节,β1-同工型依赖于存在的糖皮质激素。

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