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Some central effects of angiotensin II. Interactions with dopaminergic transmission.
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1985
Year
HypertensionPharmacotherapySocial SciencesMolecular PharmacologyDopamine SynthesisBehavioral NeuroscienceAt IiVascular PharmacologyBehavioral PharmacologyBehavioural PharmacologyNeuropharmacologyNervous SystemDopaminePharmacologyDopamine ResearchAngiotensin IiNeurophysiologyPhysiologyNeuroscienceCentral Nervous SystemMedicine
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.