Zheng Yong, Liu Zhi-quan, Ye Tao, He Lan, Wang Yi, Fang Yuan, Li Jian-ning, Liu Ping, Ye Feng
Department of Cardiology, First Hospital of Xi'an JiaoTong University, Xi'an 710061, China.
Di Yi Jun Yi Da Xue Xue Bao. 2005 Jul;25(7):827-32.
To investigate the effect of high-salt diet on blood pressure, renal morphology and osteopontin (OPN) expression in Sprague-Dawley rat with Ang II-induced renal injury.
Thirty-six male SD rats aged 12 weeks receiving normal salt diet were rolled in the study, and received Ang II (100 ng.kg-1.min-1) for two weeks using subcutaneous minipump. Rats were then fed high sodium (n=18, 4% NaCl) or normal sodium (n=18, 0.6% NaCl) diet from third week respectively and lasted for 12 weeks. Eighteen rats in the control were sham-operated and fed normal sodium diet. Tail systolic blood pressure (SBP) was determined every two weeks. Expressions of TGF-beta1 OPN mRNA and its protein in SD rat kidney were measured with quantitative RT-PCR and immunohistochemistry respectively at the end of Ang II infusion and at the end of the experiment. Renal ultrastructure was observed by electronmicroscopy.
SBP of the rats received Ang II increased significantly compared with controls (P?0.05). SBP returned to normal after Ang II infusion stopped. No significant difference existed in blood pressure between rats fed high salt diet and normal salt diet in the period of 12 weeks (P<0.05). Expressions of TGF-beta1, OPN mRNA and its protein in the kidney of the rats fed with high salt diet were up-regulated at the end of Ang II infusion (P>0.05) and at the end of the 12th week compared with the rats fed normal salt diet and controls (P<0.01). The kidney was damaged by Ang II, which was further aggravated by the infusion of high salt diet.
High salt diet could aggravate the renal injury of the rats with Ang II-induced renal injury that may be independent of blood pressure change. Expressions of the TGF-beta1, OPN mRNA and its protein were up-regulated after renal injury.
探讨高盐饮食对血管紧张素II（Ang II）诱导肾损伤的Sprague-Dawley大鼠血压、肾脏形态及骨桥蛋白（OPN）表达的影响。
选取36只12周龄雄性SD大鼠，给予正常盐饮食，采用皮下微型泵持续输注Ang II（100 ng·kg-1·min-1）2周。自第3周起，分别给予高钠（n=18，4% NaCl）或正常钠（n=18，0.6% NaCl）饮食，持续12周。18只对照大鼠行假手术并给予正常钠饮食。每2周测定尾动脉收缩压（SBP）。在Ang II输注结束时及实验结束时，分别采用定量逆转录聚合酶链反应（RT-PCR）和免疫组织化学法检测SD大鼠肾脏中转化生长因子-β1（TGF-β1）、OPN mRNA及其蛋白的表达。通过电子显微镜观察肾脏超微结构。
输注Ang II的大鼠SBP较对照组显著升高（P<0.05）。停止输注Ang II后SBP恢复正常。12周期间，高盐饮食组与正常盐饮食组大鼠血压无显著差异（P>0.05）。与正常盐饮食组大鼠及对照组相比，高盐饮食组大鼠在Ang II输注结束时（P<0.05）及第12周结束时肾脏中TGF-β1、OPN mRNA及其蛋白表达上调（P<0.01）。Ang II导致肾脏损伤，高盐饮食进一步加重肾脏损伤。
高盐饮食可加重Ang II诱导肾损伤大鼠的肾脏损伤，且可能独立于血压变化。肾脏损伤后TGF-β1、OPN mRNA及其蛋白表达上调。
