Journal of Applied Physiology Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 71: 1309-1314, 1991;
8750-7587/91 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Atzori, L.
Right arrow Articles by Moldeus, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Atzori, L.
Right arrow Articles by Moldeus, P.

Journal of Applied Physiology, Vol 71, Issue 4 1309-1314, Copyright © 1991 by American Physiological Society

ARTICLES

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 and P. Moldeus
Department of Toxicology, Karolinska Institutet, Stockholm, Sweden.

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.


This article has been cited by other articles:


Home page
 J. Am. Soc. Nephrol.Home page
A. A. Banday, F. R. Fazili, and M. F. Lokhandwala
Oxidative Stress Causes Renal Dopamine D1 Receptor Dysfunction and Hypertension via Mechanisms That Involve Nuclear Factor-{kappa}B and Protein Kinase C
J. Am. Soc. Nephrol., May 1, 2007; 18(5): 1446 - 1457.
[Abstract] [Full Text] [PDF]

Home page
 J. Pharmacol. Exp. Ther.Home page
X. J. Zhou, N. D. Vaziri, X. Q. Wang, F. G. Silva, and Z. Laszik
Nitric Oxide Synthase Expression in Hypertension Induced by Inhibition of Glutathione Synthase
J. Pharmacol. Exp. Ther., March 1, 2002; 300(3): 762 - 767.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
N. D. Vaziri, X. Q. Wang, F. Oveisi, and B. Rad
Induction of Oxidative Stress by Glutathione Depletion Causes Severe Hypertension in Normal Rats
Hypertension, July 1, 2000; 36(1): 142 - 146.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online