L-arginine causes whereas L-argininosuccinic acid inhibits endothelium-dependent vascular smooth muscle relaxation.
Biochem Biophys Res Commun
; 161(2): 536-43, 1989 Jun 15.
Article
en En
| MEDLINE
| ID: mdl-2500120
This study examined the actions of L-arginine, a putative precursor of endothelium-derived nitric oxide, and arginine analogs on endothelium-dependent relaxation of isolated rings of bovine pulmonary artery. L-Arginine did not consistently relax arterial rings unless rings were first rendered refractory to endothelium-dependent relaxation by pretreatment with 1 microM A23187 for 45 min. L-Arginine-elicited relaxation was endothelium-dependent, antagonized by oxyhemoglobin or methylene blue, and unaffected by indomethacin. L-Argininosuccinic acid caused endothelium-dependent contractions and irreversible inhibition of endothelium-dependent but not nitroglycerin-elicited relaxation, which was not overcome by addition of L-arginine. Inhibition of endothelium-dependent relaxation by L-NG-monomethyl arginine, however, was reversible and overcome by L-arginine. Therefore, endothelium-dependent relaxants may cause arginine depletion in endothelial cells and endogenous argininosuccinic acid may modulate the biosynthesis of endothelium-derived nitric oxide from arginine.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Arginina
/
Ácido Argininosuccínico
/
Endotelio Vascular
/
Músculo Liso Vascular
Tipo de estudio:
Etiology_studies
Límite:
Animals
Idioma:
En
Revista:
Biochem Biophys Res Commun
Año:
1989
Tipo del documento:
Article
Pais de publicación:
Estados Unidos