Rettig R, Speck G, Simon W, Schelling P, Fahrer A, Ganten D
Klin Wochenschr. 1978;56 Suppl 1:43-5. doi: 10.1007/BF01477451.
Cerebrospinal fluid (CSF) of rats contains high angiotensinogen concentrations. When 3500-fold purified renin from human brain was injected into the brain ventricles of rats, angiotensin I concentrations increased from undetectable levels to 147.9 +/- 18.8 fMol per ml CSF. In parallel, mean arterial blood pressure increased from 93 +/- 2.4 mm Hg to 107 +/- 3.7 mm Hg. The increase in blood pressure could be abolished by intraventricular administration of saralasin, a blocker of angiotensin II receptors. Intraventricular injection of cathepsin D had no effect on arterial blood pressure and the agiotensin I concentration in CSF remained below detection limits of the radioimmunoassay. We conclude that brain renin acts on endogenous brain angiotensinogen under physioloical in vivo conditions to form angiotensin I. The latter is converted to angiotensin II and leads to biological effects, i.e. increase of blood pressure.
大鼠的脑脊液（CSF）中含有高浓度的血管紧张素原。当将3500倍纯化的人脑肾素注入大鼠脑室时，脑脊液中血管紧张素I的浓度从无法检测的水平增加到每毫升脑脊液147.9±18.8飞摩尔。与此同时，平均动脉血压从93±2.4毫米汞柱升高到107±3.7毫米汞柱。脑室注射血管紧张素II受体阻滞剂沙拉新可消除血压升高。脑室注射组织蛋白酶D对动脉血压没有影响，脑脊液中的血管紧张素I浓度仍低于放射免疫测定的检测限。我们得出结论，脑肾素在体内生理条件下作用于内源性脑血管紧张素原以形成血管紧张素I。后者转化为血管紧张素II并导致生物学效应，即血压升高。
