Depression of Ca2+ influx in complement C5a-stimulated neutrophils by calmodulin inhibitors
The Korean Journal of Physiology and Pharmacology
;
: 109-117, 1998.
Article
in English
| 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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Trifluoperazine
/
Calmodulin
/
Complement System Proteins
/
Verapamil
/
Complement C5a
/
Chlorpromazine
/
Egtazic Acid
/
Superoxides
/
Peroxidase
/
Staurosporine
Language:
English
Journal:
The Korean Journal of Physiology and Pharmacology
Year:
1998
Type:
Article
Similar
MEDLINE
...
LILACS
LIS