Endothelin-1 (ET-1) is a more potent constrictor of femoral venous than femoral arterial smooth muscle. By contrast, endothelium-dependent contractions to anoxia are more prominent in the artery. Unlike those to ET-1, the endothelium-dependent contractions evoked by anoxia are rapid in onset and readily reversible, they are antagonized by Ca2+ entry blockers. ET-1-induced responses are inhibited by endothelium-dependent relaxing factors in canine arteries, and to a lower extent in veins. ET-1 does not augment the production of cyclic GMP in cultured porcine aortic endothelial cells, or in canine arteries and veins, suggesting that the peptide does not evoke the release of endothelium-dependent relaxing factor (EDRF) in canine blood vessels. The endothelium-derived contracting factor (EDCF) released during anoxic contraction cannot be bioassayed, under conditions where ET-1 causes contraction of the bioassay tissue. No ET-1 appears to be released in the extracellular space during anoxic contractions. These findings do not support the hypothesis that ET-1 is the EDCF released by anoxia.
|Original language||English (US)|
|Journal||Journal of Cardiovascular Pharmacology|
|State||Published - 1989|
- Arachidonic acid
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine