PGI2 production by rat blood vessels: diminished prostacyclin formation in veins compared to arteries.

Homogenates of eleven different blood vessels from normal Sprague-Dawley rats varied in their ability to produce PGI2 (i.e., 6-keto-PGF1 alpha) from [1-14C]PGH2. The most notable difference was seen between arteries and veins. Arterial tissues produced more 6-keto-PGF1alpha from exogenous PGH2 than veins at all enzyme (i.e., protein) concentrations tested. Similar results were obtained utilizing different homogenization techniques or arterial and venous rings, indicating this difference was real and not due to homogenization artifacts. In addition, the thoracic segment of the inferior vena cava was more active in converting added [1-14C-A1PGH2 to 6-keto-PGF1alpha than the abdominal segment of the inferior vena cava suggestive of a possible segmental distribution of the enzyme activity in blood vessels. These results may be interpreted as indicating that PGI2 may have a vasomotor function for blood vessels in addition to its proposed antithrombotic role.