Goldman R, Bar-Shavit Z, Romeo D
FEBS Lett. 1983 Aug 8;159(1-2):63-7. doi: 10.1016/0014-5793(83)80417-7.
Neurotensin (NT) was found to induce oriented locomotion and augment the phagocytic capability of human blood neutrophils over 10(-11) - 10(-7) M. The tridecapeptide also causes Ca2+ extrusion from neutrophils, very likely as a result of intracellular Ca2+ mobilization. It is suggested that the NT-mediated functional modulation of neutrophils correlates with the capacity of NT to affect the intracellular compartmentalization of Ca2+. Peripheral NT-elicited phenomena such as vasodilation, enhanced vascular compartmentalization of Ca2+. Peripheral NT-elicited phenomena such as vasodilation, enhanced vascular permeability, mast cell degranulation and the enhancement of directional migration and phagocytosis of neutrophils described here, classify NT as a typical mediator of inflammation.
神经降压素（NT）在浓度为10^(-11) - 10^(-7) M时，可诱导人血中性粒细胞定向运动并增强其吞噬能力。该十三肽还会导致中性粒细胞排出Ca2+，这很可能是细胞内Ca2+动员的结果。有人提出，NT介导的中性粒细胞功能调节与NT影响Ca2+细胞内区室化的能力相关。外周NT引发的现象，如血管舒张、Ca2+血管区室化增强、血管通透性增加、肥大细胞脱颗粒以及本文所述的中性粒细胞定向迁移和吞噬作用增强，将NT归类为一种典型的炎症介质。
