Apomorphine potentiates vagal bradycardia

Eur J Pharmacol. 1989 Aug 3;166(3):511-4. doi: 10.1016/0014-2999(89)90365-8.

Abstract

The effects of apomorphine, a dopamine (DA) agonist, on vagal bradycardia were investigated in chloralose-anesthetized dogs. Negative chronotropic responses to vagal nerve stimulation were significantly potentiated by apomorphine (10, 20 or 200 micrograms/kg i.v.). Pretreatment with the non-selective DA antagonist, haloperidol, or the selective DA2 antagonist, domperidone (but not the selective DA1 antagonist, SCH 23390), antagonized the effect of apomorphine. These results demonstrate that apomorphine potentiates electrically induced vagal bradycardia by a specific action on DA2 receptors which could be located on vagal nerve endings.

MeSH terms

  • Anesthesia
  • Animals
  • Apomorphine / pharmacology*
  • Benzazepines / pharmacology
  • Blood Pressure / drug effects
  • Dogs
  • Domperidone / pharmacology
  • Dopamine Antagonists
  • Female
  • Haloperidol / pharmacology
  • Heart Rate / drug effects*
  • Male
  • Vagus Nerve / physiology*

Substances

  • Benzazepines
  • Dopamine Antagonists
  • Domperidone
  • Haloperidol
  • Apomorphine