Qadri F, Badoer E, Stadler T, Unger T
Department of Pharmacology, University of Heidelberg, F.R.G.
Brain Res. 1991 Nov 1;563(1-2):137-41. doi: 10.1016/0006-8993(91)91526-7.
Interaction with aminergic transmitter substances has been implicated in the central actions of angiotensin II (ANG II). We used the novel technique of brain microdialysis in conscious rats to investigate whether ANG II influences the release of endogenous catecholamines (CA) from the anterior hypothalamus (AH). Intracerebroventricular (i.c.v.) administration of ANG II (1 ng and 100 ng) increased mean arterial pressure. ANG II at 1 ng had no effect on the release of noradrenaline (NA) from the AH but ANG II at 100 ng significantly increased NA release. Intracerebroventricular pretreatment with the ANG II-receptor antagonist sarilesin (Sar1, Ile8-ANG II; 3 micrograms) prevented the ANG II-induced NA release. The release of the intraneuronal NA and dopamine (DA) metabolites 3,4-dihydroxyphenylethyl glycol (DOPEG) and 3,4-dihydroxyphenylacetic acid (DOPAC) from the AH was not altered by i.c.v. ANG II. Our results provide the first in vivo evidence for NA release from the hypothalamus induced by periventricular ANG II receptor stimulation. They support the hypothesis that hypothalamic noradrenergic mechanisms are involved in the central actions of this peptide.
血管紧张素II(ANG II)的中枢作用与胺能递质物质的相互作用有关。我们采用脑微透析新技术,在清醒大鼠中研究ANG II是否影响下丘脑前部(AH)内源性儿茶酚胺(CA)的释放。脑室内(i.c.v.)注射ANG II(1纳克和100纳克)可提高平均动脉压。1纳克的ANG II对AH中去甲肾上腺素(NA)的释放没有影响,但100纳克的ANG II可显著增加NA的释放。用血管紧张素II受体拮抗剂sarilesin(Sar1,Ile8-ANG II;3微克)进行脑室内预处理可阻止ANG II诱导的NA释放。i.c.v.注射ANG II不会改变AH中神经元内NA和多巴胺(DA)代谢产物3,4-二羟基苯乙二醇(DOPEG)和3,4-二羟基苯乙酸(DOPAC)的释放。我们的结果首次提供了体内证据,表明脑室周围ANG II受体刺激可诱导下丘脑释放NA。这些结果支持了下丘脑去甲肾上腺素能机制参与该肽中枢作用的假说。