Korean J Physiol Pharmacol.  1998 Feb;2(1):109-117.

Depression of Ca2+ influx in complement C5a-stimulated neutrophils by calmodulin inhibitors

• Ham DS
• Kim HH
• Han ES
• Lee CS

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.

Keyword

Calmodulin inhibitors; Intracellular Ca2+ mobilization; Complement C5a; Neutrophils

MeSH Terms

Calmodulin*
Chlorpromazine
Complement C5a
Complement System Proteins*
Cytosol
Depression*
Egtazic Acid
Genistein
Imipramine
Neutrophils*
Peroxidase
Staurosporine
Superoxides
Trifluoperazine
Verapamil
Calmodulin
Chlorpromazine
Complement C5a
Complement System Proteins
Egtazic Acid
Genistein
Imipramine
Peroxidase
Staurosporine
Superoxides
Trifluoperazine
Verapamil