Nizet A
Pflugers Arch. 1979 Jan 31;378(3):223-5. doi: 10.1007/BF00592739.
The kidneys of sodium-loaded dogs, treated by indomethacin before their transplantation to the neck vessels of sodium-depleted animals, lose their ability to increase the fractional excretion of sodium following an intravenous infusion of saline; they behave similarly to the kidneys of sodium-depleted dogs. Moreover, they become unable to potentiate the response of the kidneys of the sodium-depleted perfusors. The experimental conditions exclude a direct effect of the drug eo ipso. The results indicate that renal prostaglandins are involved in the adjustment of the renal response to saline loading, depending on the previous dietary sodium balance, and that they are related with the potentiating factors released into the blood by the kidneys of sodium-loaded animals.
给钠负荷增加的狗的肾脏在移植到钠缺乏动物的颈部血管之前用消炎痛处理,在静脉输注生理盐水后,它们失去了增加钠排泄分数的能力;它们的行为与钠缺乏狗的肾脏相似。此外,它们无法增强钠缺乏灌注动物肾脏的反应。实验条件排除了药物本身的直接作用。结果表明,肾前列腺素参与了根据先前饮食钠平衡对肾脏对盐水负荷反应的调节,并且它们与钠负荷增加动物的肾脏释放到血液中的增强因子有关。