Actions of calcium influx blockers in human neutrophils support a role for receptor-operated calcium entry.
The action of two potent store operated Ca2+ entry (SOCE) inhibitors, ML-9 and GdCl3 on Ca2+ fluxes induced by the pro-inflammatory agonists FMLP, PAF, LTB(4) as well as the receptor-independent stimulus thapsigargin has not been documented in human neutrophils. In this study, ML-9 enhanced both release and subsequent Ca2+ influx in response to agonists whereas it enhanced Ca2+ release by thapsigargin, but inhibited Ca2+ influx. In contrast, 1muM GdCl3 completely inhibited Ca2+ influx in response to thapsigargin, but only partially blocked Ca2+ influx after agonist stimulation. These results strongly suggest a major role for receptor-operated Ca2+ influx in human neutrophils.
Salmon
Michael D
MD
Leukocyte and Ion Channel Research Laboratory, School of Health and Biosciences, University of East London, Stratford Campus, Romford Road, London E15 4LZ, UK.
Ahluwalia
Jatinder
J
D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D006801:Humans; D009504:Neutrophils / Q000187:drug effects* / Q000378:metabolism*; D044169:Receptors, Calcium-Sensing / Q000378:metabolism*
D002121:Calcium Channel Blockers; D044169:Receptors, Calcium-Sensing; D002118:Calcium