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

Publication ,  Journal Article
Kadowitz, PJ; McMahon, TJ; Hood, JS; Feng, CJ; Minkes, RK; Dyson, MC
Published in: J Cardiovasc Pharmacol
1991

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.

Duke Scholars

Published In

J Cardiovasc Pharmacol

DOI

ISSN

0160-2446

Publication Date

1991

Volume

17 Suppl 7

Start / End Page

S374 / S377

Location

United States

Related Subject Headings

  • Vasoconstriction
  • Respiratory System
  • Receptors, Thromboxane
  • Receptors, Prostaglandin
  • Pulmonary Circulation
  • Prostaglandin-Endoperoxide Synthases
  • Male
  • Female
  • Endothelins
  • Dose-Response Relationship, Drug
 

Citation

APA
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MLA
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Kadowitz, P. J., McMahon, T. J., Hood, J. S., Feng, C. J., Minkes, R. K., & Dyson, M. C. (1991). Pulmonary vascular and airway responses to endothelin-1 are mediated by different mechanisms in the cat. J Cardiovasc Pharmacol, 17 Suppl 7, S374–S377. https://doi.org/10.1097/00005344-199100177-00106
Kadowitz, P. J., T. J. McMahon, J. S. Hood, C. J. Feng, R. K. Minkes, and M. C. Dyson. “Pulmonary vascular and airway responses to endothelin-1 are mediated by different mechanisms in the cat.J Cardiovasc Pharmacol 17 Suppl 7 (1991): S374–77. https://doi.org/10.1097/00005344-199100177-00106.
Kadowitz PJ, McMahon TJ, Hood JS, Feng CJ, Minkes RK, Dyson MC. Pulmonary vascular and airway responses to endothelin-1 are mediated by different mechanisms in the cat. J Cardiovasc Pharmacol. 1991;17 Suppl 7:S374–7.
Kadowitz, P. J., et al. “Pulmonary vascular and airway responses to endothelin-1 are mediated by different mechanisms in the cat.J Cardiovasc Pharmacol, vol. 17 Suppl 7, 1991, pp. S374–77. Pubmed, doi:10.1097/00005344-199100177-00106.
Kadowitz PJ, McMahon TJ, Hood JS, Feng CJ, Minkes RK, Dyson MC. Pulmonary vascular and airway responses to endothelin-1 are mediated by different mechanisms in the cat. J Cardiovasc Pharmacol. 1991;17 Suppl 7:S374–S377.

Published In

J Cardiovasc Pharmacol

DOI

ISSN

0160-2446

Publication Date

1991

Volume

17 Suppl 7

Start / End Page

S374 / S377

Location

United States

Related Subject Headings

  • Vasoconstriction
  • Respiratory System
  • Receptors, Thromboxane
  • Receptors, Prostaglandin
  • Pulmonary Circulation
  • Prostaglandin-Endoperoxide Synthases
  • Male
  • Female
  • Endothelins
  • Dose-Response Relationship, Drug