1. The degradation of ADP by the placenta and umbilical artery was investigated. 2. Supernatants from incubations of finely chopped placental and umbilical arterial tissue were incubated with [ 14 C]ADP for various durations from 0 to 30 min. 3. Products of ADP degradation were separated by thin-layer chromatography and radioactivity incorporated into each product was measured. 4. Placental supernatants induced a more rapid degradation of ADP than the umbilical artery supernatants. The main product of ADP degradation by placental supernatants at 30 min was adenosine, whereas that of umbilical artery was AMP. 5. This conversion by placenta of ADP, a potent platelet aggregator and vasoconstrictor, into adenosine, a potent platelet anti-aggregator and vasodilator,-5-be important in the maintenance of perfusion of the foetoplacental unit.

1. Portal hypertension was produced experimentally in rats by partial ligation of the portal vein. 2. One week later portal veins of these animals were shown to release significantly greater amounts of prostacyclin than control animals. 3. It is postulated that if this response occurs in man, local vasodilatation and inhibition of platelet aggregation may be exacerbatory factors in the severity of haemorrhage from oesophageal varices that complicate portal hypertension.