In rat atria isolated with their cardioaccelerans nerves and labeled with [(3) H]norepinephrine, exposure to 1 x 10-7mol/L angiotensin II (Ang II) and 1 x 10-7mol/L Ang-(1-7) increased the release of radioactivity elicited by nerve stimulation (0.5-millisecond-long square-wave pulses at 2 Hz during 2 minutes) by 90% and 60%, respectively. The facilitatory effect on noradrenergic neurotransmission caused by both peptides was stereospecifically prevented by Nomega-nitro-L-arginine methyl ester (1 x 10-4mol/L), an inhibitor of nitric oxide synthase that catalyzes the conversion of L-arginine to nitric oxide, as well as by 1 x 10-5mol/L methylene blue, a substance that inhibits the guanylate cyclase considered as the final target of nitric oxide action. On the other hand, the precursor of nitric oxide synthesis, L-arginine (1 x 10-3mol/L), reversed the prevention produced by Nomega-nitro-L-arginine methyl ester on the increased release of norepinephrine caused by Ang II and Ang-(1-7). The present results suggest that nitric oxide could be involved in the neuromodulatory function elicited by both Ang II and Ang-(1-7) in rat atria. The physiological role of this observation is still under study. (Hypertension. 1997;29:1344-1350.)