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链脲佐菌素诱导的糖尿病大鼠肾小管钠泵及钠钾ATP酶增加。

Increased renal tubular sodium pump and Na+,K+-adenosine triphosphatase in streptozotocin-diabetic rats.

作者信息

Ku D D, Meezan E

出版信息

J Pharmacol Exp Ther. 1984 Jun;229(3):664-70.

PMID:6144789
Abstract

The effects of chronic glucose osmotic diuresis on renal tubular sodium pump and Na+,K+-adenosine triphosphatase (ATPase) activities were studied in chronic streptozotocin-induced diabetic rats. Four to seven weeks after streptozotocin (60 mg/kg i.p.) injection, specific renal Na+,K+-ATPase activity showed a 34.8% increase as compared to the saline-citrate treated controls, whereas the nonspecific Mg++-ATPase was not altered. The concentration of Na+,K+-ATPase, estimated from the maximum [3H]ouabain binding site concentration, also showed a significant increase in the chronic streptozotocin-diabetic rats. To determine further the specificity of this increase in Na+,K+-ATPase, the activity of the sodium pump, estimated from ouabain-sensitive 86Rb uptake, was measured in nonenzymatically isolated renal tubules. Again, a significant (+106.4%) increase in the renal tubular sodium pump activity was observed in the streptozotocin-diabetic rats, whereas the nonspecific, ouabain-insensitive 86Rb uptake was not altered. Neither was there any difference in 86Rb uptake by the isolated renal glomeruli. Thus, it appears that chronic streptozotocin-induced diabetes in rats is associated with a significant increase in renal tubular sodium pump and Na+,K+-ATPase. The latter effects may represent an important physiologic adaptation of the kidneys to maintain electrolyte homeostasis in diabetes.

摘要

在链脲佐菌素诱导的慢性糖尿病大鼠中,研究了慢性葡萄糖渗透性利尿对肾小管钠泵及钠钾 - 腺苷三磷酸酶(ATP酶)活性的影响。腹腔注射链脲佐菌素(60mg/kg)4至7周后,与生理盐水 - 柠檬酸盐处理的对照组相比,肾脏特异性钠钾 - ATP酶活性增加了34.8%,而非特异性镁离子 - ATP酶未发生改变。根据最大[3H]哇巴因结合位点浓度估算的钠钾 - ATP酶浓度,在慢性链脲佐菌素诱导的糖尿病大鼠中也显著增加。为进一步确定钠钾 - ATP酶这种增加的特异性,在非酶分离的肾小管中测量了由哇巴因敏感的86Rb摄取估算的钠泵活性。同样,在链脲佐菌素诱导的糖尿病大鼠中观察到肾小管钠泵活性显著增加(+106.4%),而非特异性、哇巴因不敏感的86Rb摄取未发生改变。分离的肾小体对86Rb的摄取也没有差异。因此,似乎链脲佐菌素诱导的大鼠慢性糖尿病与肾小管钠泵及钠钾 - ATP酶的显著增加有关。后一种效应可能代表了肾脏在糖尿病中维持电解质稳态的重要生理适应性变化。

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