Sullivan M J, Harding J W, Wright J W
Department of Psychology, Washington State University, Pullman 99164.
Brain Res. 1988 Jul 26;456(2):249-53. doi: 10.1016/0006-8993(88)90224-7.
Recent iontophoretic data suggest that conversion of angiotensin II (AII) to angiotensin III (AIII) may be necessary before the peptide can activate central angiotensin-sensitive neurons. Furthermore, this conversion may be inhibited by the aminopeptidase A inhibitor, amastatin. In the present study we investigated the importance of aminopeptidase activity on central angiotensin-induced pressor responses. Intracerebroventricular (i.c.v.) pretreatment with amastatin, suppressed i.c.v. AII-induced pressor responses. Pretreatment with the aminopeptidase B inhibitor, bestatin, increased pressor responses to AIII. Pressor responses induced by the aminopeptidase-resistant analogue, [Sar1]angiotensin II, were not affected by pretreatment with angiotensin inhibitors. These results support the hypothesis that AII must be converted to AIII to be active in the brain.
近期的离子电渗疗法数据表明，在血管紧张素II（AII）激活中枢血管紧张素敏感神经元之前，可能需要先将其转化为血管紧张素III（AIII）。此外，氨基肽酶A抑制剂氨肽菌素可能会抑制这种转化。在本研究中，我们调查了氨基肽酶活性对中枢血管紧张素诱导的升压反应的重要性。用氨肽菌素进行脑室内（i.c.v.）预处理，可抑制i.c.v. AII诱导的升压反应。用氨基肽酶B抑制剂贝抑素进行预处理，可增强对AIII的升压反应。氨基肽酶抗性类似物[Sar1]血管紧张素II诱导的升压反应不受血管紧张素抑制剂预处理的影响。这些结果支持了以下假设：AII必须转化为AIII才能在大脑中发挥作用。
