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Leu-enkephalin provokes naloxone-insensitive pulmonary vasoconstriction
Life Sciences
|March 19, 1984
Summary
Leu-enkephalin causes dose-dependent pulmonary vasoconstriction in rat lungs. This effect is not mediated by opiate, histamine, or serotonin receptors, suggesting a direct vasoconstrictor action.
Area of Science:
- Pharmacology
- Physiology
Background:
- Leu-enkephalin is an endogenous opioid peptide.
- Its effects on the pulmonary circulation are not fully understood.
Purpose of the Study:
- To investigate the mechanism of leu-enkephalin-induced pulmonary vasoconstriction in isolated perfused rat lungs.
- To determine if opiate, histamine, or serotonin receptors mediate these effects.
Main Methods:
- Isolated perfused rat lung model.
- Administration of leu-enkephalin to assess pulmonary arterial pressure.
- Use of receptor antagonists (naloxone, naltrexone, pyrilamine, methysergide) and agonists (morphine).
Main Results:
- Leu-enkephalin caused a dose-dependent increase in pulmonary arterial pressure.
- Naloxone, naltrexone, pyrilamine, and methysergide did not attenuate these pressor responses.
- Morphine did not mimic the pressor effects of leu-enkephalin.
Conclusions:
- The pulmonary vasoconstrictor effects of leu-enkephalin in isolated perfused rat lungs are not mediated by conventional opiate, histamine, or serotonin receptors.
- Leu-enkephalin may exert direct vasoconstrictor effects on the pulmonary circulation independent of these known receptor systems.