Potentiation by indomethacin of receptor-mediated catecholamine secretion in rat adrenal medulla.
Jpn J Pharmacol
; 73(3): 197-205, 1997 Mar.
Article
em En
| MEDLINE
| ID: mdl-9127814
ABSTRACT
Effects of indomethacin on catecholamine secretion evoked by receptor agonists, muscarine, bradykinin or histamine, in rat adrenal chromaffin cells were studied. Indomethacin at 200 microM increased a sustained component of secretion during stimulation with muscarine, bradykinin and histamine by a factor of 2.3, 2.1 and 2.9, respectively, whereas it did not significantly alter basal, high-K(+)- and nicotine-evoked secretions. Although indomethacin at above 400 microM dose-dependently increased basal secretion, the amount of secretion induced by indomethacin alone was much smaller than that in muscarine-evoked secretion as compared at the same concentration of indomethacin applied. Bradykinin-evoked secretion and its potentiation by indomethacin were not inhibited by 20 microM nifedipine but were suppressed by 0.5 mM Ni2+. The cyclooxygenase inhibitor, ibuprofen (200 microM) did not mimic the effect of indomethacin; prostaglandin E2 (20 microM) and arachidonic acid (100 microM) did not significantly alter either bradykinin-evoked secretion itself or its potentiation by indomethacin. Bradykinin increased the intracellular free Ca2+ concentration, [Ca2+]i, in cells loaded with indo-1, and this response was enhanced in the presence of indomethacin. These results suggest that indomethacin may promote Ca2+ entry to potentiate agonist-evoked catecholamine secretions through a novel action that is not directly related to the inhibition of cyclooxygenase activity with indomethacin.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Catecolaminas
/
Indometacina
/
Cálcio
/
Inibidores de Ciclo-Oxigenase
/
Medula Suprarrenal
Limite:
Animals
Idioma:
En
Revista:
Jpn J Pharmacol
Ano de publicação:
1997
Tipo de documento:
Article