Pulmonary vascular and airway responses to endothelin-1 are mediated by different mechanisms in the cat.

Published

Journal Article

The role of cyclooxygenase product formation and thromboxane A2 receptor activation in the response to endothelin-1 (ET-1) was investigated and compared in the airways and in the pulmonary vascular bed of the intact-chest cat. Intravenous injections of ET-1, 0.3 nmol/kg, increased lung resistance and decreased dynamic compliance. Bronchoconstrictor responses to ET-1 were decreased significantly by a cyclooxygenase inhibitor and by a thromboxane receptor blocking agent. In the pulmonary vascular bed of the cat under constant flow conditions, ET-1 increased lobar arterial pressure in a dose-related manner, and pulmonary vasconstrictor responses to the peptide were not altered by a cyclooxygenase inhibitor or thromboxane receptor blocking agent. The cyclooxygenase inhibitor blocked responses to the prostaglandin precursor, arachidonic acid; and the thromboxane receptor blocking agent reduced responses to the thromboxane mimic, U-46619. The present data suggest that bronchoconstrictor responses to ET-1 are dependent on the release of arachidonic acid, the formation of prostaglandins, and activation of thromboxane A2 receptors whereas pulmonary vasoconstrictor responses to the peptide are mediated by a different mechanism.

Full Text

Duke Authors

Cited Authors

  • Kadowitz, PJ; McMahon, TJ; Hood, JS; Feng, CJ; Minkes, RK; Dyson, MC

Published Date

  • 1991

Published In

Volume / Issue

  • 17 Suppl 7 /

Start / End Page

  • S374 - S377

PubMed ID

  • 1725384

Pubmed Central ID

  • 1725384

International Standard Serial Number (ISSN)

  • 0160-2446

Digital Object Identifier (DOI)

  • 10.1097/00005344-199100177-00106

Language

  • eng

Conference Location

  • United States