Marceau F, Bouthillier J, Tremblay B, St-Pierre S
Unité de Recherche sur l'Inflammation, C.H.U.L., Québec, Canada.
Agents Actions. 1987 Oct;22(1-2):43-9. doi: 10.1007/BF01968815.
Two small molecular weight fibrin degradation product, the pentapeptide 6A and the undecapeptide 6D, produced relaxations of norepinephrine-contracted rabbit aorta strips. The relaxations were slow-developing and were elicited by both peptides at supramicromolar concentrations; the amplitude of relaxations were small for 6D. The relaxations induced by 6A were not dependent on the presence of endothelium and were not modified by a mixture of indomethacin, pyrilamine, and cimetidine. The amplitude of the relaxations produced by 6A and 6D increased as a function of incubation time in vitro. In another experimental system, peptides 6A and 6D failed to increase 6-keto-PGF1 alpha release from cultured human umbilical endothelial cells. Histamine and bradykinin were both active in this system.
两种小分子量的纤维蛋白降解产物，五肽6A和十一肽6D，可使去甲肾上腺素收缩的兔主动脉条舒张。舒张作用发展缓慢，两种肽在超微摩尔浓度时均可引发；6D引起的舒张幅度较小。6A引起的舒张不依赖于内皮细胞的存在，且不受吲哚美辛、吡苄明和西咪替丁混合物的影响。6A和6D产生的舒张幅度随体外孵育时间而增加。在另一个实验系统中，肽6A和6D未能增加培养的人脐静脉内皮细胞释放6-酮-前列环素F1α。组胺和缓激肽在该系统中均有活性。
