Fluharty S J, Manaker S
Behav Neurosci. 1983 Oct;97(5):738-45. doi: 10.1037//0735-7044.97.5.738.
Intracerebroventricular infusion of angiotensin II (Ang II) elicits a substantial sodium appetite in the rat. The present results demonstrate that this phenomenon consists of a small, early phase of sodium ingestion that is not the result of prior sodium loss but that thereafter urinary excretion of sodium exceeds intake and consequently the animals become hyponatremic and hypovolemic. The larger and more sustained bouts of sodium ingestion occurring 8-12 hr after the start of the Ang II infusion appear to represent a behavioral compensation for this incurred sodium deficit. These results confirm the arousal of a sodium appetite by action of Ang II on the brain but indicate the need for caution in assigning to it a direct and exclusive role in the neuroendocrine control of sodium intake.
脑室内注入血管紧张素II(Ang II)会引发大鼠强烈的钠食欲。目前的结果表明,这种现象包括一个小的、早期的钠摄入阶段,这并非先前钠流失的结果,但此后钠的尿排泄超过摄入量,因此动物会出现低钠血症和血容量不足。在Ang II注入开始后8 - 12小时出现的更大且更持续的钠摄入发作似乎代表了对这种产生的钠缺乏的行为补偿。这些结果证实了Ang II作用于大脑会激发钠食欲,但也表明在将其直接且排他地归因于钠摄入的神经内分泌控制方面需要谨慎。