哇巴因对大鼠肾皮质Na^+-K^+-ATP酶活性及多巴胺D_1受体mRNA表达的影响  

Effects of ouabain on Na^+-K^+-ATPase activity and the expression of dopamine D_1 receptor in rat kidney cortex

作　　者：张玉蓉[1] 袁祖贻[2] 任延平[1] 

机构地区：[1]西安交通大学医学院第一附属医院老年内科,陕西西安710061 [2]西安交通大学医学院第一附属医院心血管内科,陕西西安710061

出　　处：《西安交通大学学报（医学版）》2010年第4期411-414,共4页Journal of Xi’an Jiaotong University（Medical Sciences）

摘　　要：目的观察哇巴因对大鼠肾皮质Na+-K+-ATP酶活性及多巴胺D1受体mRNA表达的影响。方法 28只SD大鼠随机分为2组,即哇巴因组[27.8μg/(kg·d)哇巴因腹腔注射]和对照组(生理盐水1mL/d腹腔注射),每周测量鼠尾动脉血压,共5周。于第3、5周后分2批处死动物,应用分光光度法测定各组大鼠肾皮质Na+-K+-ATP酶活性,同时采用实时定量PCR(real-timePCR)观察肾皮质中多巴胺D1受体mRNA表达的变化。结果大鼠腹腔注射哇巴因3周后,两组血压无显著性差异,但哇巴因组大鼠肾皮质Na+-K+-ATP酶活性高于对照组(P<0.01),多巴胺D1受体mRNA表达低于对照组(P<0.01)。5周后,哇巴因组大鼠血压与对照组相比有显著性差异(P<0.01),哇巴因组大鼠肾皮质Na+-K+-ATP酶活性进一步增高(P<0.01),多巴胺D1受体mRNA表达进一步减低(P<0.01)。结论长期小剂量外周注射哇巴因可使SD大鼠血压持续升高,这一作用与肾近曲小管Na+-K+-ATP酶活性增加引起水钠潴留有关,多巴胺D1受体可能参与了这一过程。Objective To study the effects of chronic ouabain treatment on Na＋-K＋-ATPase activity and the expression of dopamine D1 receptor in rat kidney cortex. Methods A total of 28 male Sprague-Dawley （SD） rats were randomly divided into ouabain group and control group,which were treated with ouabain or saline for 5 weeks; rat tail systolic blood pressure （SBP） was recorded weekly. Rats were sacrificed after 3 and 5 weeks,respectively. Then Na＋-K＋-ATPase activity and the expression of dopamine D1 receptor in rat kidney cortex were measured by colorimetric assay and real-time PCR,respectively. Results After 3 weeks of ouabain treatment,the mean SBP did not change significantly,but the Na＋-K＋-ATPase activity increased （P0.01） and the expression of dopamine D1 receptor decreased （P0.01） in comparison with those in control group. After 5 weeks,the mean SBP was significantly higher in ouabain group than in control group （P0.01）; the Na＋-K＋-ATPase activity further increased （P0.01） and the expression of dopamine D1 receptor further decreased （P0.01）. Conclusion Chronic peripheral administration of low-dose ouabain can constantly raise blood pressure of rats,which may be related to the increased renal sodium retention induced by the increased renal cortical Na＋-K＋-ATPase activity. Dopamine D1 receptor might be involved in this process.

关 键 词：Na+-K+-ATP酶活性 多巴胺D1受体 哇巴因 高血压 钠转运 

分 类 号：R363.21[医药卫生—病理学]