Wang D H, Du Y, Yao A, Hu Z
Department of Internal Medicine, Hypertension and Vascular Research Laboratories, University of Texas Medical Branch, Galveston 77555, USA.
J Hypertens. 1996 Dec;14(12):1409-15. doi: 10.1097/00004872-199612000-00004.
To test the hypothesis that a high salt intake decreases gene expression of both type 1 angiotensin receptor subtypes 1A and 1B (AT1A and AT1B) and diminishes AT1 receptor density in the kidney through an angiotensin II (Ang II)-independent mechanism.
Wistar rats were divided into four groups and fed a normal-sodium diet (0.5%, NSD), NSD + 25 ng/kg per min Ang II infusion, a high-sodium diet (4%, HSD), or HSD + Ang II infusion for 2 weeks. Quantitative reverse transcriptase-polymerase chain reaction was used for analysis of changes in renal AT1A and AT1B messenger RNA (mRNA) levels. Radioligand binding assays were used for measurement of Ang II receptor density.
Body weight and mean arterial pressure did not differ among the four groups. Renal AT1A and AT1B mRNA levels were decreased significantly in NSD + Ang II and HSD + Ang II groups compared with those in the NSD group. Renal AT1B mRNA was also decreased significantly in HSD versus NSD. The renal AT1 receptor density was decreased significantly in NSD + Ang II and HSD + Ang II, but was not changed in HSD compared with NSD.
A high salt intake downregulates the AT1B mRNA expression but does not change the AT1A mRNA expression and AT1 receptor density in the kidney, suggesting that differential regulation occurs in the kidney. Infusion of a nonpressor dose of Ang II, either alone or in conjunction with a high salt intake, downregulates the AT1 receptor and its subtype gene expression in the kidney, suggesting that Ang II regulates these responses through a negative feedback mechanism.
验证高盐摄入通过一种不依赖血管紧张素II（Ang II）的机制降低1A型和1B型血管紧张素1受体亚型（AT1A和AT1B）的基因表达并减少肾脏中AT1受体密度这一假说。
将Wistar大鼠分为四组，分别给予正常钠饮食（0.5%，NSD）、NSD + 每分钟25 ng/kg的Ang II输注、高钠饮食（4%，HSD）或HSD + Ang II输注，持续2周。采用定量逆转录聚合酶链反应分析肾脏中AT1A和AT1B信使核糖核酸（mRNA）水平的变化。采用放射性配体结合试验测量Ang II受体密度。
四组大鼠的体重和平均动脉压无差异。与NSD组相比，NSD + Ang II组和HSD + Ang II组的肾脏AT1A和AT1B mRNA水平显著降低。与NSD相比，HSD组的肾脏AT1B mRNA也显著降低。NSD + Ang II组和HSD + Ang II组的肾脏AT1受体密度显著降低，但HSD组与NSD组相比无变化。
高盐摄入下调肾脏中AT1B mRNA表达，但不改变AT1A mRNA表达和AT1受体密度，提示在肾脏中存在差异调节。单独或与高盐摄入联合输注非升压剂量的Ang II可下调肾脏中AT1受体及其亚型基因表达，提示Ang II通过负反馈机制调节这些反应。
