1. The vasoconstrictor and vasodilator activity of cultured bovine pulmonary artery endothelial cells was measured to determine how exposure to different partial pressures of O2 [Po2 142, 42 and 15 mmHg (18.9, 5.6 and 2 kPa)] affects the production of endothelial-derived relaxing and constrictor factors
2. A de-endothelialized rat aortic ring [maintained at a Po2 of 142 mmHg (18.9 kPa)] was used to bioassay the effluent from a perfused column of bovine endothelial cells grown on microcarrier beads. The endothelial cells were stimulated by 10−7 mol/l bradykinin given for 1 min at 12 min intervals
3. At the start, middle and end of the experiment the bovine endothelial cells were exposed to a Po2 of 142 mmHg (18.9 kPa) and when stimulated by bradykinin the perfusate caused respectively a 70 ± 4%, 63 ± 6% and 63 ± 6% (mean ± sem) relaxation of an aortic ring which had been pre-contracted by 10−6 mol/l phenylephrine. At a Po2 of 42 mmHg (5.6 kPa) the relaxation induced by the cells was not significantly altered, but this tailed to zero after 26–38 min exposure of the cells to a Po2 of 15 mmHg(2 kPa)
4. These responses were unaltered by the presence of 10−5 mol/l indomethacin, suggesting that prostacyclin is not a significant vasodilator in this system
5. Reduced production of endothelium-derived relaxant factor rather than production of a constrictor factor, or a direct effect on the smooth muscle, may be involved in pulmonary hypoxic vasoconstriction.