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(Hypertension. 1997;29:1344-1350.)
© 1997 American Heart Association, Inc.

Articles

Possible Participation of Nitric Oxide in the Increase of Norepinephrine Release Caused by Angiotensin Peptides in Rat Atria

M. M. Gironacci; P. S. Lorenzo; ; E. Adler-Graschinsky

From Instituto de Química y Fisicoquímica Biológicas (UBA-CONICET), Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires (M.M.G.), and Instituto de Investigaciones Farmacológicas (CONICET), Buenos Aires, Argentina.

Correspondence to Dr Edda Adler-Graschinsky, Instituto de Investigaciones Farmacológicas, Junín 956, 5^o piso, Buenos Aires (1113), Argentina. E-mail eadler{at}huemul.ffyb.uba.ar

Abstract In rat atria isolated with their cardioaccelerans nerves and labeled with [³H]norepinephrine, exposure to 1x10^-7 mol/L angiotensin II (Ang II) and 1x10^-7 mol/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 N-nitro-L-arginine methyl ester (1x10^-4 mol/L), an inhibitor of nitric oxide synthase that catalyzes the conversion of L-arginine to nitric oxide, as well as by 1x10^-5 mol/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 (1x10^-3 mol/L), reversed the prevention produced by N-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.

Key Words: nitric oxide • norepinephrine • heart rate • angiotensin II

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