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Does endothelin-1 mediate endothelium-dependent contractions during anoxia?
P M Vanhoutte1, W Auch-Schwelk, C Boulanger
1Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota 55905.
Journal of Cardiovascular Pharmacology
|January 1, 1989
Summary
Endothelin-1 (ET-1) constricts veins more than arteries, while anoxia causes rapid arterial contractions. Findings suggest ET-1 is not the endothelium-derived contracting factor released during anoxia.
Area of Science:
- Vascular biology
- Endothelium function
- Smooth muscle physiology
Background:
- Endothelin-1 (ET-1) is a potent vasoconstrictor.
- Endothelium-dependent contractions to anoxia differ between arteries and veins.
Purpose of the Study:
- To investigate the role of ET-1 in endothelium-dependent contractions induced by anoxia.
- To determine if ET-1 is the endothelium-derived contracting factor (EDCF) released during anoxia.
Main Methods:
- Comparative analysis of ET-1 and anoxia-induced contractions in femoral arteries and veins.
- Investigation of the involvement of calcium channels and endothelium-derived relaxing factors (EDRFs).
- Bioassay of potential EDCF released during anoxia.
Main Results:
- ET-1 is a more potent constrictor of venous smooth muscle than arterial smooth muscle.
- Anoxia elicits rapid, reversible, endothelium-dependent contractions in arteries, antagonized by Ca2+ entry blockers.
- ET-1 does not appear to be the EDCF released during anoxic contractions, as it could not be bioassayed under these conditions.
Conclusions:
- The findings do not support the hypothesis that ET-1 is the EDCF released by anoxia.
- Distinct mechanisms mediate ET-1-induced and anoxia-induced endothelium-dependent contractions in canine blood vessels.