In this study we tested the hypothesis that nitric oxide (NO), which function as a novel type of inter-cellular messenger in the central nervous system (CNS) participated in the facilitator effect of arginine vasopressin (AVP) on learning and memory. Recent investigations have provided evidences that inhibition of NO synthesis attenuated the vasodilatation caused by AVP, and inhibited the improvement of learning and memory evoked by angiotensin II. AVP as well as pharmacologically produced increase in endogenous NO facilitates the consolidation of shock avoidance learning. We evaluated the behavioural effects of AVP at dose 1 mug after the inhibition of NOS by N(G)-nitro-L-arginine methyl ester (L-NAME) at dose 10 mug, and after the injection of endogenous donor of NO -L-argnine- 10 mug in the retrieval of passive avoidance situation, and in consolidation of active avoidance responses. The locomotor activity of all investigated drugs was tested in the open field test. AVP facilitated the recall of passive avoidance responses and consolidation of active avoidance responses. Neither the increase of NO concentration after the injection of L-arginine nor the decrease of NO after the inhibition of NOS by L-NAME changed the behavioural effects of AVP. L-arginine increased the psychomotor behaviour and L-NAME decreased the activity of animals in the 'open field' test. L-arginine itself improved the consolidation of active avoidance responses. Our results indicate that central action of AVP is probably independent of NO concentration in the brain.