Captopril-induced enhancement of fMet-Leu-Phe-activated enzyme secretion from neutrophils.
Captopril enhanced exocytotic enzyme secretion from rabbit peritoneal neutrophils activated by suboptimal concentrations of fMet-Leu-Phe. For optimal enhancement the presence of Ca2+ was required. Captopril did not induce enzyme secretion by its own, and there was little effect on PMA-induced exocytosis. Cyclic GMP level of neutrophils was transiently enhanced by captopril. Methylene blue inhibited both captopril-induced enhancement of enzyme release and of cGMP levels. From our studies and from reports in the literature it appears that cGMP level-enhancing compounds may have both activating or inhibitory properties.
Elferink
J G
JG
Department of Medical Biochemistry, University of Leiden, The Netherlands.
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D002216:Captopril / Q000494:pharmacology*; D006152:Cyclic GMP / Q000378:metabolism; D004357:Drug Synergism; D004789:Enzyme Activation / Q000187:drug effects; D005089:Exocytosis / Q000187:drug effects; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology*; D009504:Neutrophils / Q000187:drug effects / Q000201:enzymology*; D011817:Rabbits
D000894:Anti-Inflammatory Agents, Non-Steroidal; D009240:N-Formylmethionine Leucyl-Phenylalanine; D002216:Captopril; D006152:Cyclic GMP