Thiol modification in H2O2- and thromboxane-induced vaso- and bronchoconstriction in rat perfused lung

L. Atzori, K. Olafsdottir, A. M. Corriga, G. Bannenberg, A. Ryrfeldt, P. Moldeus*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

23 Citations (Scopus)

Abstract

Hydrogen peroxide (H2O2), arachidonic acid (AA), and U-44069, a thromboxane analogue, all induced vaso- and bronchoconstriction in the isolated perfused rat lung. The role of protein sulfhydryl modifications in these processes was investigated. The thiol oxidizing agent diamide inhibited both vaso- and bronchoconstriction induced by H2O2, AA, or U-44069. Diamide had only a marginal effect on glutathione and protein thiol levels and no effect on lung mechanics. The diamide inhibition was reversible, and H2O2-induced vaso- and bronchoconstriction was almost maximal after 10 min of perfusion with buffer. The recovery was more rapid if dithiothreitol, a thiol reducing agent, was used in the buffer. H2O2- and AA-induced vaso- and bronchoconstriction is caused by thromboxane release. Diamide did not influence H2O2- or AA-dependent thromboxane formation, indicating that neither AA release nor AA metabolism to thromboxane is sensitive to thiol oxidation. Thus our results indicate that the site of diamide-induced thiol oxidation is the thromboxane receptor or its signal transduction.

Original languageEnglish
Pages (from-to)1309-1314
Number of pages6
JournalJournal of Applied Physiology
Volume71
Issue number4
DOIs
Publication statusPublished - 1991

Other keywords

  • arachidonic acid
  • diamide
  • dithiothreitol
  • signal transduction
  • thromboxane receptor

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