Effect of hypoxia on prostacyclin production in cultured pulmonary artery endothelium

Michael C. Madden, Robert L. Vender, Mitchell Friedman

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


Exposure of cultured bovine pulmonary artery endothelial cells to varying levels of hypoxia (10% or 0% O2) for 4 hours resulted in a significant dose-dependent inhibition in endothelial prostacyclin synthesis (51% and 98%, at the 10% and 0% O2 levels respectively, p <0.05, compared to 21% O2 exposure values). Release of 3H-arachidonic acid from cellular pools was not altered by hypoxia. Some of the cells were incubated with arachidonic acid (20 μM for 5 min) or PGH2 (4 μM for 2 min) immediately after exposure. Endothelium exposed to 0% O2, but not to 10% O2, produced significantly less prostacyclin after addition of either arachidonic acid (25 ± 5% of 21% O2 exposure values, n=6, p <0.01) or PGH2 (31 ± 3% of 21% O2 exposure values, n=6, p <0.05). These results suggest that hypoxia inhibits cyclooxygenase at the 10% O2 level and both cyclooxygenase and prostacyclin synthetase enzymes at the 0% O2 exposure levels. Exposure of aortic endothelial cells resulted in a 44% inhibition of prostacyclin at the 0% exposure level. No significant alteration in prostacyclin production was found in pulmonary vascular smooth muscle cells exposed to hypoxia. These data suggest that the increased prostacyclin production reported in lungs exposed to hypoxia is not due to a direct effect of hypoxia on the main prostacyclin producing cells of the pulmonary circulation.

Original languageEnglish (US)
Pages (from-to)1049-1062
Number of pages14
Issue number6
StatePublished - Jun 1986

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Endocrinology


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