Schelling P, Ganten U, Sponer G, Unger T, Ganten D
Neuroendocrinology. 1980 Nov;31(5):297-308. doi: 10.1159/000123092.
From the in vitro and in vivo measurements of the components of the renin-angiotensin system (RAS) in the cerebrospinal fluid (CSF) of rats and dogs, it was concluded that angiotension II (ANG II) is not generated within the CSF in significant amounts, since renin was found to be unmeasurable in CSF under most circumstances. The specific concentrations of angiotensinogen and of converting enzyme (CE) were high. Angiotensin I (ANG I) concentrations were low in CSF, while ANG II levels were comparable to those measured in plasma under control conditions. Neither ANG I nor ANG II penetrated from the blood into the brain ventricles of rats, provided that no unrealistically high doses of ANG II were administered intravenously. This holds true even if high blood pressure increases were induced by intravenous ANG II infusion in deoxycorticosterone acetate (DOCA) and salt-treated rats. However, increased ANG II concentrations were measured in CSF perfusate, when the blood-brain barrier (BBB) was opened by the intracarotid injection of a hyperosmolar urea solution. The brain ventricular perfusion of increasing concentrations of ANG II revealed constant recovery of less than 40%. CSF did not contain angiotensinase activity, but ANG II degradation was high in some periventricular regions. ANG II, the ANG II antagonist saralasin, and the CE inhibitor captopril, respectively, escaped from CSF into circulation when high doses of these substances were applied intraventricularly. We conclude that ANG II in the CSF does not originate from and is not related to plasma ANG II. It is probably not generated within the CSF. ANG II may be synthetized in the brain tissue and be released into the brain ventricles where its rapid degradation occurs in contact with circumventricular structures.
通过对大鼠和犬脑脊液（CSF）中肾素 - 血管紧张素系统（RAS）各成分进行体外和体内测量，得出的结论是，脑脊液中不会大量生成血管紧张素II（ANG II），因为在大多数情况下，脑脊液中的肾素含量无法检测到。血管紧张素原和转化酶（CE）的特定浓度较高。脑脊液中血管紧张素I（ANG I）浓度较低，而在对照条件下，ANG II水平与血浆中测得的水平相当。只要静脉内不给予过高剂量的ANG II，ANG I和ANG II都不会从血液渗入大鼠脑室。即使通过静脉内输注ANG II在醋酸脱氧皮质酮（DOCA）和盐处理的大鼠中诱导血压升高，情况也是如此。然而，当通过颈内注射高渗尿素溶液打开血脑屏障（BBB）时，在脑脊液灌流液中测得ANG II浓度升高。向脑室灌注浓度不断增加的ANG II显示，回收率始终低于40%。脑脊液中不含有血管紧张素酶活性，但在一些脑室周围区域，ANG II的降解程度较高。当向脑室内应用高剂量的ANG II、ANG II拮抗剂沙拉新和CE抑制剂卡托普利时，它们分别从脑脊液逸出进入循环。我们得出结论，脑脊液中的ANG II并非源自血浆ANG II，也与之无关。它可能不是在脑脊液中生成的。ANG II可能在脑组织中合成，并释放到脑室中，在那里与室周结构接触时会迅速降解。
