Effect of captopril on the bradykinin-induced release of prostacyclin from guinea-pig lungs and bovine aortic endothelial cells.

1. In guinea-pig isolated lungs perfused with Krebs solution, captopril (10 microM) inhibited the metabolism of bradykinin (Bk) and the conversion of angiotensin I to angiotensin II, as measured by bioassay. Captopril significantly enhanced Bk-stimulated output of prostacyclin. 2. In bovine aortic endothelial cells grown on microcarrier beads, captopril (10 microM) did not affect the release of prostacyclin or of endothelium-derived relaxing factor (EDRF) induced by Bk. 3. Angiotensin I or angiotensin II did not release prostacyclin from guinea-pig isolated lungs or bovine aortic endothelial cells. They were also ineffective as releasers of EDRF from bovine aortic endothelial cells. 4. Thus, activation of angiotensin converting enzyme is not involved in the release of prostacyclin from guinea-pig isolated lungs or bovine aortic endothelial cells, or in release of EDRF from bovine aortic endothelial cells.