Chodobski A, Szmydynger-Chodobska J, Segal M B, McPherson I A
Department of Clinical and Applied Physiology, Institute of Physiological Sciences, School of Medicine, Warsaw, Poland.
Brain Res. 1992 Oct 23;594(1):40-6. doi: 10.1016/0006-8993(92)91027-c.
The effect of central and peripheral administrations of angiotensin II (AII) on cerebrospinal fluid (CSF) formation was investigated in rabbits anesthetized with intravenous alpha-chloralose and urethane. CSF production was measured by the ventriculo-cisternal perfusion method with Blue dextran 2000 used as an indicator substance. AII infused intracerebroventricularly (i.c.v.) at rates of 5.5 and 55 pg min-1 significantly decreased CSF formation rate by 27% and 36%, respectively. This AII action could be completely blocked by simultaneously administered specific AII antagonist, [Sar1,Ala8]AII (saralasin), given i.c.v. at a rate of 5.5 ng min-1. Intracerebroventricular infusion of AII at a rate of 5.5 ng min-1 did not change CSF production. Saralasin, when given alone into the ventricular system (5.5 ng min-1), non-significantly increased CSF production by 12%. However, in 4 of the 6 animals studied, the rise in CSF production was statistically significant (by 23%). Intravenous infusion of AII at rates of 30 and 100 ng kg-1 min-1 was found not to change CSF formation rate. Also, i.c.v. administration of angiotensin I converting enzyme inhibitor, captopril (10 microliters min-1), did not influence CSF production. It is concluded that the centrally released AII can control CSF production. Our results suggest that under normal conditions, AII exerts a tonic inhibitory effect on CSF formation. In contrast, the blood-borne peptide seems not to influence this physiological process.
在静脉注射α-氯醛糖和乌拉坦麻醉的家兔中，研究了中枢和外周给予血管紧张素II（AII）对脑脊液（CSF）生成的影响。以蓝色葡聚糖2000作为指示物质，采用脑室-脑池灌注法测量CSF生成量。以5.5和55 pg min-1的速率脑室内（i.c.v.）注入AII，分别使CSF生成速率显著降低27%和36%。同时以5.5 ng min-1的速率脑室内给予特异性AII拮抗剂[Sar1,Ala8]AII（沙拉新），可完全阻断AII的这一作用。以5.5 ng min-1的速率脑室内注入AII对CSF生成无影响。单独将沙拉新注入脑室系统（5.5 ng min-1）时，CSF生成量非显著性增加12%。然而，在6只研究动物中的4只，CSF生成量的增加具有统计学意义（增加23%）。发现以30和100 ng kg-1 min-1的速率静脉注入AII不会改变CSF生成速率。此外，脑室内给予血管紧张素I转换酶抑制剂卡托普利（10微升min-1）不影响CSF生成。得出的结论是，中枢释放的AII可控制CSF生成。我们的结果表明，在正常情况下，AII对CSF生成发挥着紧张性抑制作用。相比之下，血源性肽似乎不影响这一生理过程。
