Flow-induced prostacyclin production is mediated by a pertussis toxin-sensitive G protein.
Fluid flow and several other agonists induce prostacyclin (PGI2) production in endothelial cells. G proteins mediate the response of a large number of hormones such as histamine, but the transduction pathway of the flow signal is unclear. We found that GDP beta S and pertussis toxin inhibited flow-induced prostacyclin production in human umbilical vein endothelial cells. In addition, flow potentiated the histamine-induced production of PGI2. This suggests that flow stimulates prostacyclin production via a pertussis toxin-sensitive G protein and modulates the stimulus-response coupling of other agonists.
Berthiaume
F
F
Department of Chemical Engineering, Pennsylvania State University, University Park 16802.
Frangos
J A
JA
D001696:Biomechanical Phenomena; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism*; D011464:Epoprostenol / Q000096:biosynthesis*; D019204:GTP-Binding Proteins / Q000037:antagonists & inhibitors / Q000502:physiology*; D006153:Guanosine Diphosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D006801:Humans; D037342:Pertussis Toxin; D013873:Thionucleotides / Q000494:pharmacology; D014471:Umbilical Veins; D010566:Virulence Factors, Bordetella / Q000494:pharmacology
D013873:Thionucleotides; D010566:Virulence Factors, Bordetella; D006153:Guanosine Diphosphate; C032829:6-thioguanosine 5'-diphosphate; D011464:Epoprostenol; D037342:Pertussis Toxin; D019204:GTP-Binding Proteins