Abstract: | The formation of prostacyclin (PGI2) and thromboxane A2 (TXA2) (measured as the stable metabolites 6-keto-PGF1α and TXB2) during stimulation with vasoactive autocoids was registered in human umbilical arteries perfused
. Responses were registered within 3–4 minutes after addition of the subtances. Both angiostensin I and II were found to increase the formation of PGI2 while depressing that of TXA2. Serotonin increased the formation of TXA2 but not that of PGI2. Both PGE2 and PGF2α stimulated the PGI2 formation. The TXA2 mimetic U46619, increased PGI2 production, whereas PGI2 slighlty increased the formation of TXA2. All responses were found to be completely inhibited by indomethacin. |