论文部分内容阅读
为了解肾病时钠储留的机制，采用配伍组设计的方法，研究了肾素－血管紧张素－醛固酮系统（ＲＡＡＳ）在阿霉素肾病大鼠肾钠储留中的作用。结果表明，接受阿霉素的所有大鼠在尿蛋白排泄增加之前，即开始肾钠潴留，切除肾上腺不能阻止其发生；出现大量蛋白尿后，醛固酮不能进一步增加钠潴留，而血管紧张素ＩＩ肽拮抗剂也不能减少钠潴留。所有肾病大鼠肾内髓匀浆中的钠－钾－三磷酸腺苷酶的活性均增加，切除肾上腺不能阻止其增加，醛固酮也不能使之进一步增加。提示ＲＡＡＳ在阿霉素肾病大鼠钠潴留的过程中不发挥作用；内髓集合管细胞上的钠－钾－三磷酸腺苷酶不再受醛固酮的调节。
In order to understand the mechanism of sodium retention during nephropathy, the effect of renin-angiotensin-aldosterone system (RAAS) on renal sodium retention in adriamycin-induced nephropathy rats was studied using a matched group design. The results showed that all adriamycin-receiving rats started renal sodium retention before removal of urinary protein excretion and removal of the adrenal gland did not prevent it; after a large amount of proteinuria, aldosterone did not further increase sodium retention, whereas angiotensin II peptide Antagonists also do not reduce sodium retention. All nephrotic rats had increased activity of sodium-potassium-adenosine triphosphatase in the nephrinous homogenate, and removal of the adrenal gland did not prevent its increase, nor did aldosterone increase it. These results suggest that RAAS does not play a role in sodium retention in adriamycin-induced nephropathy rats; sodium-potassium-ATPase in medullary collecting tube cells is no longer regulated by aldosterone.