Depression of Ca2+ influx in complement C5a-stimulated neutrophils by calmodulin inhibitors.
- Author:
Dong Suk HAM
1
;
Hyun Ho KIM
;
Eun Sook HAN
;
Chung Soo LEE
Author Information
1. Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul 156-756, Korea.
- Publication Type:Original Article
- Keywords:
Calmodulin inhibitors;
Intracellular Ca2+ mobilization;
Complement C5a;
Neutrophils
- MeSH:
Calmodulin*;
Chlorpromazine;
Complement C5a;
Complement System Proteins*;
Cytosol;
Depression*;
Egtazic Acid;
Genistein;
Imipramine;
Neutrophils*;
Peroxidase;
Staurosporine;
Superoxides;
Trifluoperazine;
Verapamil
- From:The Korean Journal of Physiology and Pharmacology
1998;2(1):109-117
- CountryRepublic of Korea
- Language:English
-
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.
