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