POSSIBLE PARTICIPATION OF NITRIC-OXIDE IN THE INCREASE OF NOREPINEPHRINE RELEASE CAUSED BY ANGIOTENSIN PEPTIDES IN RAT ATRIA

In rat atria isolated with their cardioaccelerans nerves and labeled w ith [H-3]norepinephrine, exposure to 1 x 10(-7) mol/L angiotensin II ( Ang II) and 1 x 10(-7) mol/L Ang-(1-7) increased the release of radioa ctivity elicited by nerve stimulation (0.5-millisecond-long square-wav e pulses at 2 Hz during 2 minutes) by 90% and 60%, respectively. The f acilitatory effect on noradrenergic neurotransmission caused by both p eptides was stereospecifically prevented by N-omega-nitro-L-arginine m ethyl ester (1 x 10(-4) mol/L), an inhibitor of nitric oxide synthase that catalyzes the conversion of L-arginine to nitric oxide, as well a s by 1 x 10(-5) mol/L methylene blue, a substance that inhibits the gu anylate cyclase considered as the final target of nitric oxide action. On the other hand, the precursor of nitric oxide synthesis, L-arginin e (1 x 10(-3) mol/L), reversed the prevention produced by N-omega-nitr o-L-arginine methyl ester on the increased release of norepinephrine c aused by Ang II and Ang-(1-7). The present results suggest that nitric oxide could be involved in the neuromodulatory function elicited by b oth Ang II and Ang-(1-7) in rat atria. The physiological role of this observation is still under study.