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Apomorphine potentiates vagal bradycardia
P Montastruc1, C Damase-Michel, J L Montastruc
1Laboratoire de Pharmacologie Médicale et Clinique INSERM U317, Faculté de Médecine, Toulouse, France.
European Journal of Pharmacology
|August 3, 1989
Summary
Apomorphine, a dopamine agonist, enhances vagal bradycardia in dogs. This effect is mediated through dopamine D2 receptors, suggesting a role in regulating heart rate.
Area of Science:
- Cardiovascular Physiology
- Neuropharmacology
- Autonomic Nervous System Research
Background:
- Vagal bradycardia is a key mechanism for regulating heart rate.
- Dopamine agonists can influence cardiovascular function.
- The specific role of dopamine receptors in vagal nerve activity requires further elucidation.
Purpose of the Study:
- To investigate the effects of apomorphine, a dopamine agonist, on vagal bradycardia in anesthetized dogs.
- To determine the involvement of specific dopamine receptor subtypes in apomorphine's action on vagal bradycardia.
Main Methods:
- Electrically induced vagal nerve stimulation in chloralose-anesthetized dogs.
- Administration of apomorphine at varying doses (10, 20, 200 µg/kg i.v.).
- Pharmacological blockade using selective and non-selective dopamine antagonists (haloperidol, domperidone, SCH 23390).
Main Results:
- Apomorphine significantly potentiated negative chronotropic responses to vagal stimulation.
- The non-selective dopamine antagonist haloperidol and the selective D2 antagonist domperidone blocked apomorphine's effect.
- The selective D1 antagonist SCH 23390 did not antagonize apomorphine's potentiation of vagal bradycardia.
Conclusions:
- Apomorphine potentiates vagal bradycardia through a specific action on dopamine D2 receptors.
- These findings suggest that dopamine D2 receptors may be located on vagal nerve endings.
- This study highlights a novel mechanism for dopamine in modulating cardiac autonomic control.