Depression of Ca2+ influx in complement C5a-stimulated neutrophils by calmodulin inhibitors
The Korean Journal of Physiology and Pharmacology
;
: 109-117, 1998.
Artigo
em Inglês
| WPRIM
| ID: wpr-728153
ABSTRACT
Role of Ca2+/calmodulin complex in intracellular Ca2+ mobilization in neutrophils has not been clearly elucidated. In this study, effects of chlorpromazine, trifluoperazine and imipramine on the intracellular Ca2+ mobilization, including Ca2+ influx, in C5a-activated neutrophils were investigated. Complement C5a-stimulated superoxide production and myeloperoxidase release in neutrophils were inhibited by chlorpromazine, trifluoperazine and imipramine, except no effect of imipramine on myeloperoxidase release. A C5a-elicited elevation of (Ca2+)i in neutrophils was inhibited by chlorpromazine, trifluoperazine, imipramine, staurosporine, genistein, EGTA, and verapamil but not affected by pertussin toxin. The intracellular Ca2+ release in C5a-activated neutrophils was not affected by chlorpromazine and imipramine. Chlorpromazine and imipramine inhibited Mn2+ influx by C5a-activated neutrophils. Thapsigargin-evoked Ca2+ entry was inhibited by chlorpromazine, trifluoperazine, imipramine, genistein, EGTA and verapamil, while in the activation process of neutrophils. The depressive action of calmodulin inhibitors on the elevation of cytosolic Ca2+ level in C5a-activated neutrophils appears to be accomplished by inhibition of Ca2+ influx from the extracellular medium.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Trifluoperazina
/
Calmodulina
/
Proteínas do Sistema Complemento
/
Verapamil
/
Complemento C5a
/
Clorpromazina
/
Ácido Egtázico
/
Superóxidos
/
Peroxidase
/
Estaurosporina
Idioma:
Inglês
Revista:
The Korean Journal of Physiology and Pharmacology
Ano de publicação:
1998
Tipo de documento:
Artigo
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