Abstract
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 language | English (US) |
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Pages (from-to) | H139-H147 |
Journal | American Journal of Physiology - Heart and Circulatory Physiology |
Volume | 267 |
Issue number | 1 36-1 |
DOIs | |
State | Published - 1994 |
Keywords
- endothelin-1
- endothelium-derived relaxing factor
- nitric oxide
- pulmonary artery
- pulmonary vein
ASJC Scopus subject areas
- Physiology
- Cardiology and Cardiovascular Medicine
- Physiology (medical)