Cyclic AMP inhibits chemotactic-peptide-induced but not Ca2+-ionophore- or tetradecanoylphorbol-acetate-induced enzyme secretion in guinea pig neutrophils.
cAMP-increasing agents such as prostaglandin El, dibutyryl cAMP and 8-bromo-cAMP inhibited N-acetyl-beta-D-glucosaminidase secretion induced by the chemotactic peptide formylmethionyl-leucyl-phenylalanine in guinea pig neutrophils. However, they could not inhibit but rather potentiated the secretion significantly when secretion was induced by the Ca2+ ionophore A23187. Similarly, these agents did not inhibit tetradecanoylphorbol acetate (TPA)-induced secretion. Moreover, the secretion induced by combined treatment with Ca2+ ionophore A23187 and TPA was hardly blocked by cAMP-increasing agents. These results strongly suggest that cAMP inhibits the secretion through suppression of a signal transduction from receptor activation to events such as Ca2+ mobilization and protein kinase C activation, probably of the inositol phospholipid metabolism.
Wada
Y
Y
Research Laboratories, Shionogi & Co., Ltd., Osaka, Japan.
D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology; D000527:Alprostadil / Q000494:pharmacology; D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D000001:Calcimycin / Q000494:pharmacology*; D000242:Cyclic AMP / Q000494:pharmacology*; D006168:Guinea Pigs; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology*; D009504:Neutrophils / Q000187:drug effects* / Q000201:enzymology; D015398:Signal Transduction / Q000187:drug effects; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*
D015124:8-Bromo Cyclic Adenosine Monophosphate; D000001:Calcimycin; D009240:N-Formylmethionine Leucyl-Phenylalanine; D003994:Bucladesine; D000242:Cyclic AMP; D000527:Alprostadil; D013755:Tetradecanoylphorbol Acetate