Hafström I, Ringertz B, Lundeberg T, Palmblad J
Department of Rheumatology, Karolinska Institutet, Stockholm Söder Hospital, Sweden.
Acta Physiol Scand. 1993 Jul;148(3):341-6. doi: 10.1111/j.1748-1716.1993.tb09565.x.
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).
神经肽被认为是炎症的介质。在生理浓度下,P物质已被证明能引发多形核中性粒细胞(PMN)的化学发光(CL)。在本研究中,我们还表明内皮素和神经肽Y(NPY),但降钙素基因相关肽(CGRP)不能引发PMN的氧化代谢。在相似的纳摩尔浓度下,P物质和内皮素(但不是NPY)也能引发甲酰甲硫氨酰亮氨酰苯丙氨酸(fMLP)诱导的细胞溶质钙升高。另一方面,NPY导致细胞溶质钙浓度直接且与剂量相关的增加。在广泛的浓度范围(1 fM - 1 microM)内,上述神经肽均不能引发PMN聚集或直接诱导CL、聚集或趋化性。