抄録
Ca2+ chylating reagent (Ethylene glycol-bis (aminoethyl ether) tetra acetic acid; EGTA), Voltage dependent Ca2+ channel blocker (Verapamil) and calmoduline antagonist (Trifluoperazine; TFP) were tested to evaluate the influence of Ca2+ on the O-2 production of leukocyte stimulated by formyl-methionyl-leucyl-phenyl-alanine (FMLP), concanavalin A (Con A) and cytochalasin D (Cyt D) . EGTA inhibited O-2 production stimulated by Con A+Cyt D and Cyt D+FMLP but did not inhibit significantly it stimulated only by FMLP. EGTA did not inhibit depolarization but inhibited repolarization of membrane potential by the stimulants described above. These facts made us believe the significance of intra-and extra-cellular Ca2+ Verapamil inhibited O-2 production only with a slight change of depolarization. These facts made us thought that Ca2+ might influx into cells depending on the change of membrane potential. And since Verapamil inhibited O-2 production only at a high concentration, it could not be used clinically as an anti-inflammatory reagent. TFP inhibited O-2 production but had nonspecific action other than a calmoduline inhibitor. So the involvement of calmoduline on O-2 production and change of membrane potential was not clear.
