Georgiev V, György L, Getova D, Markovska V
Acta Physiol Pharmacol Bulg. 1985;11(4):19-26.
The effects of angiotensin II (AT II) administered intracerebroventricularly (i.c.v.) on some behavioural reactions were studied. AT II increased the electroshock convulsive-seizure threshold in mice. Sulpiride antagonized this effect of AT II. AT II increased the exploratory behaviour of rats in open field. This effect was potentiated by nomifensine (a dopamine uptake blocker) and was blocked by haloperidol. AT II increased apomorphine stereotypy and the effect was antagonized by saralasin and haloperidol and partly by alpha-methyl-para-tyrosine (alpha-MpT) (an inhibitor of dopamine synthesis). AT II decreased the locomotor activity of mice. At doses of 0.5 and 1 microgram per mouse AT II did not change haloperidol (5 mg/kg)- or tetrabenazine (25 mg/kg)-induced catalepsy. It is assumed that the behavioural effects of AT II are realized through angiotensin receptors and through interactions between these receptors and dopaminergic transmission in the brain structures involved in the behavioural reactions studied.
研究了脑室内注射血管紧张素II（AT II）对某些行为反应的影响。AT II提高了小鼠的电休克惊厥阈值。舒必利拮抗AT II的这种作用。AT II增加了大鼠在旷场中的探究行为。诺米芬辛（一种多巴胺摄取阻滞剂）增强了这种作用，而氟哌啶醇则阻断了这种作用。AT II增加了阿扑吗啡刻板行为，这种作用被沙拉新和氟哌啶醇拮抗，部分被α-甲基对酪氨酸（α-MpT，一种多巴胺合成抑制剂）拮抗。AT II降低了小鼠的自发活动。每只小鼠注射0.5微克和1微克剂量的AT II时，并未改变氟哌啶醇（5毫克/千克）或丁苯那嗪（25毫克/千克）诱导的僵住症。推测AT II的行为效应是通过血管紧张素受体以及这些受体与参与所研究行为反应的脑结构中多巴胺能传递之间的相互作用实现的。
