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神经肽Ｐ物质能激活多种参与炎症和免疫反应的细胞．然而Ｐ物质直接刺激人粒细胞产生超氧阴离子（Ｏ÷２）需要较高的浓度（＞１０μｍｏｌ·Ｌ－１）．本实验观察了低浓度Ｐ物质对人粒细胞超氧阴离子生成的活化作用．结果表明，Ｐ物质在低浓度时（３μｍｏｌ·Ｌ－１）能活化人粒细胞，使甲酰基－甲硫氨酰基－亮氨酰基苯丙氨酸（ｆＭＬＰ）刺激产生的超氧阴离子明显增多．Ｐ物质的这一活化作用呈剂量和时间依赖性．在无细胞外钙的情况下，Ｐ物质没有这种活化作用．Ｐ物质活化ｆＭＬＰ引起的Ｏ÷２生成增多作用可被神经激肽（ＮＫ）－１受体阻断剂ｓｐｅｎｔｉｄｅ（１μｍｏｌ·Ｌ－１），磷脂酶Ｃ抑制剂Ｕ－７３１２２（１０ｎｍｏｌ·Ｌ－１）以及Ｃａ２＋通道阻断剂尼卡地平（１μｍｏｌ·Ｌ－１）所抑制．这些发现提示，Ｐ物质活化人粒细胞可能是经ＮＫ－１受体偶联的磷脂酰肌醇代谢途径，并且是细胞外钙依赖性的
Neuropeptide substance P activates a wide variety of cells involved in inflammation and immune responses. However, substance P directly stimulates human granulocytes to produce superoxide anion (O ÷ 2) at higher concentrations (> 10 μmol·L -1). This experiment observed the effect of substance P on the production of superoxide anion of human granulocyte. The results showed that substance P activated human granulocytes at low concentration (3μmol·L-1), and the superoxide anion produced by fMLP stimulated the production of superoxide anion. This activation of substance P is dose and time dependent. Substance P does not have this activation without extracellular calcium. The increase of O ÷ 2 production induced by substance-activated fMLP could be inhibited by spentide (1μmol·L-1), phosphorylase C inhibitor U-73122 (10nmol·L-1) ) And Ca2 + channel blocker nicardipine (1μmol·L-1). These findings suggest that substance P-activated human granulocytes may be the phosphatidylinositol metabolic pathway that is coupled via the NK-1 receptor and is extracellularly calcium-dependent