肾血管性高血压大鼠肾脏A型心房肽受体的表达及意义

Expression of A-type Atrial Natriuretic Peptide Receptor in the Kidneys of Renovascular Hypertension Rats and Its Implication

目的研究高血压大鼠肾脏A型心房肽受体(ANPR-A)的蛋白表达并探讨其意义。方法采用狭窄单侧肾动脉的方法建立二肾一夹(2K 1C)肾血管性高血压大鼠模型。用尾套法测血压,免疫组织化学染色法观察缩窄术后不同时期肾脏组织各部位ANPR-A蛋白的表达,并用计算机图像分析系统半定量检测ANPR-A蛋白的表达水平。结果肾动脉缩窄术后4周,模型组大鼠肾脏ANPR-A蛋白在肾小球表达增加,在肾小管表达降低,与对照组的差异有统计学意义(P<0.01),在髓质集合管表达无明显改变(P>0.05)。缩窄术后8周,模型组大鼠肾脏ANPR-A蛋白在肾小管和髓质集合管的表达均降低,与对照组的差异有统计学意义(P<0.01),在肾小球有微弱表达,与对照组相比差异无统计学意义(P>0.05)。结论随着高血压的发展,肾脏组织中的ANPR-A表达显著减少,提示高血压的发展与肾脏ANPR-A的表达下降有关。

Objective To investigate the expression of A-type atrial natriuretic peptide receptor （ANPR-A） in the kidneys of renovascular hypertension rats and evaluate the significance of the expression. Methods The rat model of renovascular hypertension was produced by constricting one lateral renal artery. After the renal artery being constricted for 4 weeks and 8 weeks, the systolic BP of rats was measured with a manometer using the tail-cuff method. Then, the expression of ANPR-A was respectively detected by immunohistochemical technique in the kidneys of the two-kidney,one-clip （2K1C） rats, and the expression level of ANPR-A was semi-quantltatlvely measured by Mias-2000 computer image analyzer. Results At 4 weeks after the artery-constricted operation, the expression of ANPR-A increased significantly in 2K1C hypertensive rat glomeruli and decreased significantly in renal tubules, compared with control（P〈0.01）, but there was no marked change in medullar collecting tubules. At 8 weeks after the artery-constricted operation, the expression of ANPR-A decreased significantly in 2K1C hypertensive rat renal tubules and medullar collecting tubules, compared with control（P〈0.01）; however, there was weak expression in glomeruli, and no statistically significant difference was seen when compared with control （P〉0. 05）. Conclusion The expression of ANPR-A decreased significantly in kidney tissues of renovascular hypertension rats, which suggested that the down-regulation of ANPR-A might be involved in the development of hypertension.