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Related Experiment Videos

Modulation of baroreflex and baroreceptor function in experimental heart failure.

I H Zucker1, W Wang

  • 1Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha.

Basic Research in Cardiology
|January 1, 1991
PubMed
Summary

Heart failure depresses baroreceptor sensitivity, impairing reflex control of circulation. This study suggests increased Na-K ATPase activity in baroreceptors contributes to this dysfunction in heart failure.

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Area of Science:

  • Cardiovascular Physiology
  • Autonomic Nervous System Regulation
  • Heart Failure Pathophysiology

Background:

  • Reflex control of circulation is abnormal in heart failure.
  • Baroreflex control of heart rate is known to be depressed in heart failure.
  • Mechanisms underlying these baroreflex abnormalities remain unclear.

Purpose of the Study:

  • Investigate the mechanisms of arterial baroreflex dysfunction in chronic heart failure.
  • Determine the roles of different components in the baroreflex arc.
  • Examine baroreceptor sensitivity and autonomic control of heart rate.

Main Methods:

  • Utilized a canine model of chronic heart failure induced by ventricular pacing.
  • Recorded arterial baroreceptor activity and constructed pressure-discharge curves.

Related Experiment Videos

  • Evaluated baroreflex control of heart rate using pharmacological agents.

    • Main Results:

    • Baroreceptor discharge sensitivity was significantly depressed in dogs with heart failure.
    • Ouabain perfusion normalized baroreceptor function, suggesting Na-K ATPase involvement.
    • Both reflex tachycardia and bradycardia were blunted in heart failure, with autonomic contributions.

    Conclusions:

    • Increased Na-K ATPase activity in baroreceptor nerve endings likely contributes to reduced sensitivity in heart failure.
    • Autonomic nervous system dysfunction plays a role in the depressed baroreflex control of heart rate.
    • Further research is needed to fully elucidate baroreflex arc abnormalities in heart failure.