Quinacrine increases endothelial nitric oxide release: role of superoxide anion.
Eur J Pharmacol
; 436(3): 159-63, 2002 Feb 02.
Article
em En
| MEDLINE
| ID: mdl-11858795
ABSTRACT
The effect of acute quinacrine treatment on agonist-induced nitric oxide (NO) release was investigated in cultured human endothelial cells using electrochemical monitoring of the in situ NO concentration. Quinacrine dose-dependently increased NO release with an apparent EC50 of 0.2 microM and a maximal effect at 1 microM. Quinacrine did not modify the dependence of NO release on extracellular L-arginine. Acceleration or deceleration of O2- dismutation, which altered NO release in control cells, did not modify it in quinacrine-treated cells. Quinacrine did not modify NO amperometric signal or reaction with O2- produced by xanthine oxidation. In the presence of quinacrine, agonist-induced NO release became Mg2+ -independent and could not be attributed to an inhibition of phospholipase A2 activity. Quinacrine made NO release insensitive to Cu2+ chelation. The present study demonstrates that acute treatment by low quinacrine concentrations increases endothelial NO release, possibly through an inhibition of O2- production.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Quinacrina
/
Endotélio Vascular
/
Óxido Nítrico
Limite:
Humans
Idioma:
En
Revista:
Eur J Pharmacol
Ano de publicação:
2002
Tipo de documento:
Article