Effect of hypoxia on prostacyclin production in cultured pulmonary artery endothelium

Michael C. Madden, Robert Vender, Mitchell Friedman

Research output: Contribution to journalArticle

41 Citations (Scopus)

Abstract

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
JournalProstaglandins
Volume31
Issue number6
DOIs
StatePublished - Jan 1 1986

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Epoprostenol
Pulmonary Artery
Endothelium
Arachidonic Acid
Prostaglandin H2
Endothelial cells
Prostaglandin-Endoperoxide Synthases
Endothelial Cells
Lung
Pulmonary Circulation
Vascular Smooth Muscle
Smooth Muscle Myocytes
Muscle
Hypoxia
Cells
Enzymes

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Endocrinology

Cite this

Madden, Michael C. ; Vender, Robert ; Friedman, Mitchell. / Effect of hypoxia on prostacyclin production in cultured pulmonary artery endothelium. In: Prostaglandins. 1986 ; Vol. 31, No. 6. pp. 1049-1062.
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abstract = "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.",
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Effect of hypoxia on prostacyclin production in cultured pulmonary artery endothelium. / Madden, Michael C.; Vender, Robert; Friedman, Mitchell.

In: Prostaglandins, Vol. 31, No. 6, 01.01.1986, p. 1049-1062.

Research output: Contribution to journalArticle

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N2 - 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.

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