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.

1. Female rats were injected with ethinyloestradiol, norethisterone or both compounds for 30 days. Prostacyclin-like activity was measured in the thoracic aorta and inferior vena cava. 2. In the thoracic aorta of rats injected with ethinyloestradiol and ethinyloestradiol/norethisterone, prostacyclin-like activity was significantly increased. Norethisterone alone had no effect. 3. In the inferior vena cava of rats injected with ethinyloestradiol, norethisterone or both compounds, prostacyclin-like activity was not significantly altered. The amount of prostacyclin generated by the inferior vena cava was much lower than that by the aorta. 4. Experimentally induced changes in the vessel wall after the administration of contraceptive steroids must be due to factors other than diminished prostacyclin production.