Release of vasodilator prostaglandin, PGI2, from isolated rat lung during vasoconstriction

Prostaglandins are generated by the lungs and released into the circulation. Since inhibitors of prostaglandin synthesis enhance hypoxic pulmonary vasoconstriction, we wondered whether vasodilator prostacyclin was synthesized by the lungs in response to vasoconstriction. To test this hypothesis, we...

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Bibliographic Details
Published in:Circulation research 1981-02, Vol.48 (2), p.207-213
Main Authors: Voelkel, N F, Gerber, J G, McMurtry, I F, Nies, A S, Reeves, J T
Format: Article
Language:English
Subjects:
Angiotensin II - pharmacology
Animals
Arachidonic Acids - metabolism
Arachidonic Acids - pharmacology
Epoprostenol - biosynthesis
Epoprostenol - pharmacology
Erythrocytes - metabolism
Lung - blood supply
Lung - metabolism
Male
Meclofenamic Acid - pharmacology
Oxygen - physiology
Perfusion
Prostaglandins - biosynthesis
Pulmonary Artery - physiology
Rats
Sodium Chloride
Vasoconstriction
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Summary:Prostaglandins are generated by the lungs and released into the circulation. Since inhibitors of prostaglandin synthesis enhance hypoxic pulmonary vasoconstriction, we wondered whether vasodilator prostacyclin was synthesized by the lungs in response to vasoconstriction. To test this hypothesis, we measured vasoconstriction induced by angiotensin II in isolated rat lungs before and after inhibition of prostaglandin synthetase. We found that sodium meclofenamate enhanced and prostacyclin and its precursor arachidonate abolished pulmonary vasoconstriction. In lungs labeled with 14C-arachidonate, effluent radioactivity increased after angiotensin II-induced vasoconstriction. Hypoxic vasoconstriction, but not hypoxia per se, caused an increase in lung effluent radioactivity. Chromatographic analysis of lung effluent showed that 6-keto-prostaglandin F1 alpha was the major arachidonic acid metabolite released during pulmonary vasoconstriction. We concluded that prostacyclin is produced by the lungs in response to vasoconstriction. Hypoxia per se seems not to be the adequate stimulus for enhanced lung prostacyclin formation. Lung prostacyclin may protect the pulmonary circulation against excessive vasoconstriction.
ISSN:0009-7330
1524-4571
DOI:10.1161/01.RES.48.2.207