Inhibitors of platelet aggregation in the fetoplacental unit and myometrium with particular reference to the ADP-degrading property of placenta.
Extracts of fresh tissue from the feto-placental unit and myometrium were tested for their ability to inhibit ADP-induced platelet aggregation and to degrade ADP. Placental extracts caused rapid reversal of aggregation and degraded ADP, both effects being mimicked by HPAP. However, whereas the latter was inhibited by L-phenylalanine but not by heating to 65 degrees C for 5 minutes, the reverse was true for crude placental extracts. Umbilical cord vessels and myometrium totally inhibited platelet aggregation in a similar way to pure PGI2. Both tissues also exhibited ADP-ase activity but were much less potent in this respect than placenta. In the system used, little or no anti-aggregatory activity was detected in extracts of non-vascular cord tissue, fetal membranes or amniotic fluid, although the two latter tissues had a weak ADP-degrading effect. Thus, it appears that in contrast to myometrium and umbilical cord vessels, the major inhibitor of platelet aggregation in placenta is an ADP-ase and not PGI2. While part of the inhibitory effect of placenta may be due to HPAP, other ADP-degrading enzymes also seem to contribute to the overall anti-aggregatory property of this organ.
D000469:Alkaline Phosphatase / Q000494:pharmacology; D001081:Apyrase / Q000032:analysis*; D011464:Epoprostenol / Q000032:analysis*; D005260:Female; D006358:Hot Temperature; D006801:Humans; D009215:Myometrium / Q000201:enzymology; D010649:Phenylalanine / Q000494:pharmacology; D010744:Phosphoric Monoester Hydrolases / Q000032:analysis*; D010920:Placenta / Q000201:enzymology*; D010974:Platelet Aggregation / Q000187:drug effects*; D011247:Pregnancy; D011453:Prostaglandins / Q000032:analysis*; D014472:Umbilicus / Q000201:enzymology
D011453:Prostaglandins; D010649:Phenylalanine; D011464:Epoprostenol; D000469:Alkaline Phosphatase; D010744:Phosphoric Monoester Hydrolases; D001081:Apyrase