Hoffman W E, Phillips M I
Brain Res. 1976 Jul 9;110(2):313-30. doi: 10.1016/0006-8993(76)90405-4.
Angiotensin II injected in small doses into the cerebral ventricles produces an increase in blood pressure and drinking behavior. The site of action for both of these effects was studied in 3 main experiments. (1) The response to several doses of angiotensin delivered to each ventricle was investigated with multiple ventricular cannulation. This revealed that the rostral ventricular system was involved in angiotensin II mediated responses. (2) CSF flow was limited by plugging specific anterior and posterior ventricular regions and then testing for angiotensin II induced drinking and pressor responses. This technique showed that the ventral anterior third ventricle must be reached by the peptide in order to produce either blood pressure or drinking effects. (3) In order to separate pressor components due to vasopressin release and sympathetic activation, hypophysectomized rats were also tested. The experiment showed that the pressor response to intraventricular angiotensin II is due to both sympathetic and pituitary hormonal components and both are dependent on sites sensitive to angiotensin in the anterior third ventricule. The ventral anterior third ventricle or periventricular tissue surrounding it seems to be essential for both blood pressure and drinking responses to intraventricular angiotensin II.
向脑室注射小剂量血管紧张素II会使血压升高并引发饮水行为。在3个主要实验中研究了这两种效应的作用位点。(1)通过多脑室插管研究了向每个脑室注射几种剂量血管紧张素后的反应。这表明,嘴侧脑室系统参与了血管紧张素II介导的反应。(2)通过堵塞特定的前、后脑室区域来限制脑脊液流动,然后测试血管紧张素II诱导的饮水和升压反应。该技术表明,该肽必须到达腹侧前三脑室才能产生血压或饮水效应。(3)为了区分由于血管加压素释放和交感神经激活引起的升压成分,还对垂体切除的大鼠进行了测试。实验表明,对脑室内血管紧张素II的升压反应是由交感神经和垂体激素成分共同引起的,两者都依赖于前三脑室中对血管紧张素敏感的位点。腹侧前三脑室或其周围的室周组织似乎对脑室内血管紧张素II引起的血压和饮水反应都至关重要。