Wald H, Popovtzer M M
Pflugers Arch. 1984 May;401(1):97-100. doi: 10.1007/BF00581539.
Renal sodium handling and microsomal Na+-K+-ATPase activity in kidney cortex, medulla and papilla of rats with streptozotocin-induced diabetes mellitus (DM) was studied. During 7 days following the administration of streptozotocin GFR, urinary excretion, filtered load and tubular reabsorption of Na+ averaged (mean +/- SE) 1.18 +/- 0.016 ml/min, 1.74 +/- 0.14, 177.3 +/- 8.9 and 175.6 +/- 8.9 mEq/min respectively in experimental rats as compared to corresponding rates of 0.85 +/- 0.04 (P less than 0.001), 0.85 +/- 0.03 (P less than 0.001), 129.8 +/- 5.8 (P less than 0.001) and 129 +/- 5.8 (P less than 0.001) respectively in the control rats. The activity of microsomal Na-K-ATPase in the kidney cortex, medulla and papilla of the control group was (mean +/- SE) 44.7 +/- 1.7, 150 +/- 7.5 and 37.4 +/- 3.6 (mumoles Pi/mg prot/h) respectively. 24 h after DM induction Na-K-ATPase activity in the cortex rose to 59.3 +/- 2.4 (P less than 0.001) and remained high after 3 and 7 days. Medullary Na-K-ATPase activity was unchanged 24 h after streptozotocin administration but was markedly increased to 260 +/- 9 (P less than 0.001) after 3 days and remained high after 7 days. These findings show that streptozotocin-induced DM in rats causes a substantial increase in GFR which is associated with a net increase in filtered and reabsorbed load of Na+ and natriuresis. These alterations are accompanied by a marked increase in Na-K-ATPase activity in renal medulla and in the cortex.
研究了链脲佐菌素诱导的糖尿病(DM)大鼠肾皮质、髓质和乳头体中的肾钠处理及微粒体Na⁺-K⁺-ATP酶活性。链脲佐菌素给药后7天内,实验大鼠的肾小球滤过率(GFR)、尿排泄、滤过负荷和钠的肾小管重吸收平均(均值±标准误)分别为1.18±0.016 ml/min、1.74±0.14、177.3±8.9和175.6±8.9 mEq/min,而对照组相应速率分别为0.85±0.04(P<0.001)、0.85±0.03(P<0.001)、129.8±5.8(P<0.001)和129±5.8(P<0.001)。对照组肾皮质、髓质和乳头体中微粒体Na-K-ATP酶的活性分别为(均值±标准误)44.7±1.7、150±7.5和37.4±3.6(微摩尔无机磷/毫克蛋白/小时)。糖尿病诱导24小时后,皮质中的Na-K-ATP酶活性升至59.3±2.4(P<0.001),并在3天和7天后仍保持较高水平。链脲佐菌素给药24小时后,髓质中的Na-K-ATP酶活性未发生变化,但3天后显著升高至260±9(P<0.001),并在7天后仍保持较高水平。这些发现表明,链脲佐菌素诱导的大鼠糖尿病导致GFR大幅增加,这与钠的滤过和重吸收负荷净增加以及利钠作用有关。这些改变伴随着肾髓质和皮质中Na-K-ATP酶活性的显著增加。