Interaction among ET-1, endothelium-derived nitric oxide, and prostacyclin in pulmonary arteries and veins

T. M. Zellers, J. McCormick, Y. Wu

Research output: Contribution to journalArticlepeer-review

82 Scopus citations


Endothelin-1 causes vasodilation of the intact porcine pulmonary vascular bed. To determine the cause of this vasodilation, we investigated the interactions of endothelin-1 (ET-1), endothelium-derived nitric oxide (EDNO), and prostacyclin in isolated small porcine pulmonary arteries and veins under in vitro conditions. ET-1 caused concentration-dependent contractions in arteries and veins, augmented by the nitric oxide synthase (NOS) inhibitor, N(ω)-nitro-L-arginine, in pulmonary veins. BQ-123 (ET(A)-receptor antagonist) depressed the ET-1-induced contractions. Sarafotoxin S6C, an ET(B)-receptor agonist, caused contractions of pulmonary veins only. Endothelium-dependent relaxations to bradykinin and ET-1 were greater in pulmonary veins compared with arteries, inhibited by N(ω)-nitro-L-arginine, and reversed by L-arginine. BQ-123 augmented ET-1-induced arterial relaxation. ET-3 and sarafotoxin S6C, ET(B)-receptor agonists, caused comparable endothelium-dependent relaxations in arteries and veins. ET-1 caused a fourfold greater increase in prostacyclin release in pulmonary veins compared with arteries. We conclude that ET-1 is a potent vasoconstrictor of porcine pulmonary vessels and stimulates the release of EDNO and prostacyclin, which oppose the contractions to the peptide. The release of these endothelium-derived vasodilators appears greater in pulmonary veins.

Original languageEnglish (US)
Pages (from-to)H139-H147
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number1 36-1
StatePublished - 1994


  • endothelin-1
  • endothelium-derived relaxing factor
  • nitric oxide
  • pulmonary artery
  • pulmonary vein

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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