Possible participation of nitric oxide in the increase of norepinephrine release caused by angiotensin peptides in rat atria.
Hypertension
; 29(6): 1344-50, 1997 Jun.
Article
in En
| MEDLINE
| ID: mdl-9180639
In rat atria isolated with their cardioaccelerans nerves and labeled with [3H]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 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 omega-nitro-L-arginine methyl 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 as by 1 x 10(-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 (1 x 10(-3) mol/L), reversed the prevention produced by N omega-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.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Peptide Fragments
/
Sympathomimetics
/
Angiotensin II
/
Norepinephrine
/
Nitric Oxide
Limits:
Animals
Language:
En
Journal:
Hypertension
Year:
1997
Document type:
Article
Affiliation country:
Argentina
Country of publication:
United States