Nickel inhibits urocortin-induced relaxation in the rat pulmonary artery.
Eur J Pharmacol
; 488(1-3): 169-72, 2004 Mar 19.
Article
em En
| MEDLINE
| ID: mdl-15044048
ABSTRACT
Urocortin relaxes rat pulmonary arteries partly through a cyclic AMP-dependent but Ca(2+) channel-independent mechanism. However, other participating mechanisms are relatively unknown. The present study was designed to examine whether the forward mode of Na(+)-Ca(2+) exchangers play a role in the relaxant responses to urocortin in isolated rat small pulmonary arteries. Endothelium-denuded rings were mounted on small vessel myographs for measurement of changes in isometric tension. Urocortin inhibited 9,11-dideoxy-11alpha,9alpha-epoxy-methanoprostaglandin F(2alpha) (U46619)-induced contraction in a concentration-dependent manner and this inhibition was reversed by astressin, a corticotropin-releasing factor receptor antagonist. Micromolar concentrations of nickel (Ni(2+)) chloride, a putative inhibitor of the Na(+)-Ca(2+) exchanger, reduced the relaxant responses to urocortin. Urocortin-induced relaxation was abolished in a Na(+)-free solution, a condition that eliminates influence of the forward mode of Na(+)-Ca(2+) exchanger. In contrast, the relaxant responses to atrial natriuretic peptide or forskolin were unaffected by Ni(2+) or with removal of extracellular Na(+). The present results provide indirect evidence suggesting that stimulation of Na(+)-Ca(2+) exchangers may contribute to urocortin-induced endothelium-independent pulmonary artery relaxation.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Artéria Pulmonar
/
Hormônio Liberador da Corticotropina
/
Músculo Liso Vascular
/
Níquel
Limite:
Animals
Idioma:
En
Ano de publicação:
2004
Tipo de documento:
Article