Cyclic AMP inhibition of fMet-Leu-Phe-dependent metabolic responses in human neutrophils is not due to its effects on cytosolic Ca2+.
Cyclic AMP powerfully inhibits the fMet-Leu-Phe-dependent respiratory burst and exocytosis of azurophilic and specific granules without affecting Ca2+ release from intracellular stores. The elevation of [Ca2+]i induced by fMet-Leu-Phe is short-lived in cyclic AMP-treated cells and similar to that of untreated cells stimulated in the absence of external Ca2+. Nevertheless, in these latter cells fMet-Leu-Phe induces metabolic activation. We therefore suggest that the inhibitory action of cyclic AMP on neutrophil responses is not due to its effects on [Ca2+]i homoeostasis.
D003994:Bucladesine / Q000494:pharmacology; D002118:Calcium / Q000097:blood*; D000242:Cyclic AMP / Q000494:pharmacology*; D003600:Cytosol / Q000378:metabolism; D005966:Glucuronidase / Q000097:blood; D006801:Humans; D066298:In Vitro Techniques; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000037:antagonists & inhibitors*; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects; D011485:Protein Binding / Q000187:drug effects; D014805:Vitamin B 12 / Q000097:blood
D009240:N-Formylmethionine Leucyl-Phenylalanine; D003994:Bucladesine; D000242:Cyclic AMP; D005966:Glucuronidase; D014805:Vitamin B 12; D002118:Calcium