Abstract
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 GDPβS 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.
Original language | English (US) |
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Pages (from-to) | 277-279 |
Number of pages | 3 |
Journal | FEBS Letters |
Volume | 308 |
Issue number | 3 |
DOIs | |
State | Published - Aug 24 1992 |
Externally published | Yes |
All Science Journal Classification (ASJC) codes
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology
Keywords
- Endothelial cell
- G protein
- Histamine
- Pertussis toxin
- Prostacyclin
- Shear stress