Prostacyclin release induced by neurokinins in cultured human endothelial cells.
The effects of neurokinins (NK) and related peptides on the secretion of 6-keto-prostaglandin F1 alpha, a stable metabolite of prostacyclin, were measured. These peptides enhanced three- to five-fold the basal secretion rate with the following rank order of potency (based on threshold concentrations for a significant output): substance P (SP) greater than or equal to NKA greater than SP 4-11 greater than or equal to [pGlu6]SP 6-11 = SP 7-11.NKB and SP 1-9 were inactive. Ac[Arg6, Sar9, Met(O2)11]SP, a NK1 receptor selective agonist, was more potent than other selective agonists for the NK2 and NK3 receptor subtypes. These results suggest that the NK receptors, which mediate the release of prostacyclin from human endothelial cells, belong to the NK1 subtype.
Marceau
F
F
Unité de recherche inflammation et immuno-rhumatologie, Centre Hospitalier de l'Université Laval, Ste. Foy, Québec, Canada.
Tremblay
B
B
Couture
R
R
Regoli
D
D
D015121:6-Ketoprostaglandin F1 alpha / Q000494:pharmacology; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism*; D011464:Epoprostenol / Q000378:metabolism*; D006801:Humans; D015288:Neurokinin A / Q000494:pharmacology*; D015287:Neurokinin B / Q000494:pharmacology*; D013373:Substance P / Q000494:pharmacology
D013373:Substance P; D015121:6-Ketoprostaglandin F1 alpha; D015288:Neurokinin A; D015287:Neurokinin B; D011464:Epoprostenol