The effect of endothelin, neuropeptide Y, calcitonin gene-related peptide and substance P on neutrophil functions.
Neuropeptides are putative mediators of inflammation. At physiological concentrations substance P has been shown to prime polymorphonuclear neutrophil granulocyte (PMN) chemiluminescence (CL). In the present study we show also that both endothelin and neuropeptide Y (NPY), but not calcitonin gene-related peptide (CGRP) are able to prime PMN oxidative metabolism. At similar nanomolar concentrations SP and endothelin (but not NPY) also primed formyl-methionyl-leucyl-phenylalanine (fMLP)-induced rises of cytosolic calcium. On the other hand, NPY caused a direct and dose-related increase of cytosolic calcium concentrations. None of the mentioned neuropeptides primed PMN aggregation or directly induced CL, aggregation or chemotaxis over a wide range of concentrations (1 fM-1 microM).
Hafström
I
I
Department of Rheumatology, Karolinska Institutet, Stockholm Söder Hospital, Sweden.
Ringertz
B
B
Lundeberg
T
T
Palmblad
J
J
D015740:Calcitonin Gene-Related Peptide / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002449:Cell Aggregation / Q000187:drug effects; D002634:Chemotaxis, Leukocyte / Q000187:drug effects; D016232:Endothelins / Q000494:pharmacology; D016257:Fura-2; D006801:Humans; D066298:In Vitro Techniques; D008163:Luminescent Measurements; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009478:Neuropeptide Y / Q000494:pharmacology; D009479:Neuropeptides / Q000494:pharmacology*; D009504:Neutrophils / Q000187:drug effects* / Q000378:metabolism; D010084:Oxidation-Reduction; D015398:Signal Transduction / Q000187:drug effects; D013373:Substance P / Q000494:pharmacology
D016232:Endothelins; D009478:Neuropeptide Y; D009479:Neuropeptides; D013373:Substance P; D009240:N-Formylmethionine Leucyl-Phenylalanine; D015740:Calcitonin Gene-Related Peptide; D002118:Calcium; D016257:Fura-2