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Related Experiment Videos

Mechanism of decrease in heart rate by peripheral dopaminergic D2-receptors

J H Yoon1, C M Ko, Y S Ahn

  • 1Department of Internal Medicine, Wonju College of Medicine, Yonsei University, Republic of Korea.

Yonsei Medical Journal
|December 1, 1994
PubMed
Summary
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Lisuride activates cardiac D2-receptors, decreasing heart rate. This effect is enhanced by higher norepinephrine levels in the synaptic cleft, distinct from alpha 2-receptors.

Area of Science:

  • Pharmacology
  • Cardiovascular Physiology
  • Neuroscience

Background:

  • The role of cardiac sympathetic nerve endings in heart rate regulation is complex.
  • Dopamine receptors (D2-receptors) have been implicated in cardiovascular control, but their specific function on cardiac sympathetic nerves requires further elucidation.
  • Understanding the interplay between neurotransmitter concentrations and receptor activity is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the heart rate-decreasing effect mediated by D2-receptors on cardiac sympathetic nerve endings.
  • To determine the relationship between D2-receptor activity and norepinephrine concentration in synaptic clefts.
  • To differentiate the D2-receptor's action from that of presynaptic alpha 2-receptors.

Main Methods:

Related Experiment Videos

  • Utilized pithed Sprague-Dawley rats to control for systemic influences.
  • Induced increased heart rate via electrical stimulation of the cardiac accelerator nerve or intravenous infusions of norepinephrine, tyramine, or isoproterenol.
  • Administered lisuride and antagonist drugs (sulpiride, yohimbine, SCH 23390) to assess receptor involvement and effects on heart rate and neurotransmitter levels.

Main Results:

  • Lisuride dose-dependently decreased heart rate, an effect blocked by sulpiride (D2 antagonist) but not yohimbine (alpha 2 antagonist) or SCH 23390 (D1 antagonist).
  • Clonidine (alpha 2 agonist) decreased heart rate, an effect blocked by yohimbine but not sulpiride, confirming alpha 2-receptor involvement.
  • Lisuride's heart rate-lowering effect was more pronounced when synaptic norepinephrine concentrations were elevated (norepinephrine and tyramine infusions) compared to when they were not (isoproterenol infusion).

Conclusions:

  • A distinct D2-receptor exists on cardiac sympathetic nerve endings that mediates a decrease in heart rate.
  • This D2-receptor-mediated effect is pharmacologically different from the presynaptic alpha 2-receptor.
  • The efficacy of D2-receptor stimulation by lisuride is potentiated by increased norepinephrine concentrations within the synaptic cleft.