Does leukotriene C4 mediate hypoxic vasoconstriction in isolated ferret lungs?

C. M. Tseng, M. McGeady, T. Privett, A. Dunn, J. T. Sylvester

Research output: Contribution to journalArticlepeer-review

Abstract

To evaluate leukotriene (LT) C4 as a mediator of hypoxic pulmonary vasoconstriction, we examined the effects of FPL55712, a putative LT antagonist, and indomethacin, a cyclooxygenase inhibitor, on vasopressor responses on LTC4 and hypoxia (inspired O2 tension = 25 Torr) in isolated ferret lungs perfused with a constant flow (50 ml·kg-1·min-1). Pulmonary arterial injections of LTC4 caused dose-related increases in pulmonary arterial pressure during perfusion with physiological salt solution containing Ficoll (4 g/dl). FPL55712 caused concentration-related inhibition of the pressor response to LTC4 (0.6 μg). Although 10 μg/ml FPL55712 inhibited the LTC4 pressor response by 61%, it did not alter the response to hypoxia. At 100 μg/ml, FPL55712 inhibited the responses to LTC4 and hypoxia by 73 and 71%, respectively, but also attenuated the vasoconstrictor responses to prostaglandin F(2α) (78% at 8 μg), phenylephrine (68% at 100 μg), and KCl (51% at 40 mM). At 0.5 μg/ml, indomethacin significantly attenuated the pressor response to arachidonic acid but did not alter responses to LTC4 or hypoxia. These results suggest that in isolated ferret lungs 1) the vasoconstrictor response to LTC4 did not depend on release of cyclooxygenase products and 2) LTC4 did not mediate hypoxic vasoconstriction.

Original languageEnglish (US)
Pages (from-to)253-259
Number of pages7
JournalJournal of applied physiology
Volume68
Issue number1
DOIs
StatePublished - 1990

Keywords

  • FPL55712
  • arachidonic acid
  • indomethacin
  • phenylephrine
  • potassium chloride
  • prostaglandin F(2α)
  • pulmonary circulation

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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