Steele T H, Gottstein J H, Challoner-Hue L
Can J Physiol Pharmacol. 1982 Oct;60(10):1311-4. doi: 10.1139/y82-193.
We examined the action of angiotensin II (AII) on isolated rat kidney perfused with a recirculating cell-free solution at either 12 pKa (90 mmHg) or 17 kPa (128 mmHg). The renal perfusion pressure was maintained constant while sufficient AII was added to increase the renal vascular resistance by 50%. In the low-pressure kidneys. AII increased the glomerular filtration rate (GFR) by 155%, increased sodium reabsorption by 157%, and decreased the urine sodium concentration by 34% without affecting sodium excretion. In the high-pressure kidneys, GFR initially was significantly greater but was not affected by AII. In these experiments, AII had no effect on sodium reabsorption or excretion and decreased the urine sodium concentration by 7%. The data suggest that AII could be involved in autoregulation of the GFR without producing large changes in sodium excretion.
我们研究了血管紧张素II（AII）对在12 pKa（90 mmHg）或17 kPa（128 mmHg）下用无细胞循环溶液灌注的离体大鼠肾脏的作用。在维持肾灌注压恒定的同时，添加足够的AII以使肾血管阻力增加50%。在低压肾脏中，AII使肾小球滤过率（GFR）增加155%，钠重吸收增加157%，尿钠浓度降低34%，而不影响钠排泄。在高压肾脏中，GFR最初显著更高，但不受AII影响。在这些实验中，AII对钠重吸收或排泄没有影响，尿钠浓度降低了7%。数据表明，AII可能参与GFR的自身调节，而不会使钠排泄发生大的变化。
