摘要
目的观察κ阿片受体激动剂U50,488H对大鼠的利尿作用并探讨其作用机制。方法用生理学整体实验技术观察U50,488H对尿量的影响;分离大鼠肾动脉,用血管环方法测定肾血管张力的变化;应用放射免疫分析方法观察其对血浆中抗利尿激素(ADH)、血管紧张素Ⅱ(AngⅡ)和心房钠尿肽(ANP)的影响。结果静脉注射U50,488H可显著增加大鼠的尿量,并且使大鼠血浆ADH水平显著性下降;在离体水平,U50,488H可以剂量依赖性地舒张大鼠的肾动脉。以上效应均可被κ阿片受体选择性阻断剂(nor-BNI)所阻断。结论U50,488H通过激动κ阿片受体使大鼠的尿量增加,舒张肾动脉和降低ADH的分泌是其利尿的主要机制。
Objective To investigate the diuretic effects of U50, 488H （trans-3, 4-dichloro- N-[2-（1- pyrrolidinyl）cyclohexyl] benzeacetamidel）, a selective κ-opioid receptor agonist, on the rats and explore the underlying mechanism. Methods The physiological experimental technique was used to collect the urine and to determine the volume of urine output; isolated artery perfusion technique was used to investigate the direct action of 050,488H on renal artery of rats; the RIA （radioimmunoassay） was used to determine the effects of 050,448H on the plasma level of some humoral factors. Results Systemic administration of U50,488H significantly increased the urine volume; the renal artery was dilated dose-dependently by 050,488H; 050,488H produced marked decrease in plasma concentration of antidiuretic hormone （ADH） in rats. These effects were abolished by norbinaltorphimine （nor-BNI）, a selective κ-opioid receptor antagonist. Conclusion U50, 488H increases the urinary volume by activation of the κ -opioid receptor in the rats. Relaxing the renal artery and decreasing plasma concentration of ADH are the main underlying mechanism.
出处
《西安交通大学学报（医学版）》
CAS
CSCD
北大核心
2005年第6期541-544,共4页
Journal of Xi’an Jiaotong University（Medical Sciences）
基金
全军医药卫生科研基金军队"十五"计划面上项目(No.01MB129)
国家自然科学基金项目(No.30370580)
关键词
Κ阿片受体
肾动脉
利尿
抗利尿激素
κ-opioid receptor
renal artery
diuresis
antidiuretic hormone（ADH）
