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Chronic beta-adrenoceptor blockade prevents the development of beta-adrenergic subsensitivity in experimental

C S Liang1, R P Frantz, M Suematsu

  • 1Department of Medicine, University of Rochester Medical Center, N.Y. 14642.

Circulation
|July 1, 1991
PubMed
Abstract

Insights

Beta-receptor blockade with nadolol prevented reduced myocardial beta-receptor density and cardiac beta-adrenergic sensitivity in dogs with right heart failure. This suggests excessive sympathetic stimulation contributes to receptor changes in heart failure.

Area of Science:

  • Cardiology
  • Pharmacology
  • Physiology

Background:

  • Congestive heart failure involves reduced myocardial beta-adrenergic receptor density and responsiveness due to excessive sympathetic stimulation.
  • Understanding the role of sympathetic overactivity in heart failure pathophysiology is crucial.

Purpose of the Study:

  • To investigate whether beta-receptor blockade can prevent myocardial changes associated with excessive sympathetic stimulation in right heart failure.

Main Methods:

  • Experimental right heart failure was induced in dogs and treated with the beta-receptor blocker nadolol (40 mg/day) for 5 weeks.
  • Control groups included sham-operated dogs and animals with right heart failure not receiving nadolol.
  • Hemodynamic parameters, plasma norepinephrine, and myocardial beta-receptor and adenylate cyclase activity were assessed.

Main Results:

  • Nadolol treatment did not prevent right ventricular hypertrophy or elevated plasma norepinephrine in heart failure.
  • However, nadolol prevented the reduction in myocardial beta-receptor density and attenuated the decrease in cardiac beta-adrenergic sensitivity.
  • No significant changes in myocardial beta-receptor or adenylate cyclase activity were observed in sham-operated dogs after nadolol treatment.

Conclusions:

  • Excessive sympathetic stimulation plays a significant role in the development of beta-receptor downregulation and subsensitivity in right heart failure.
  • Beta-receptor blockade may offer a therapeutic strategy to preserve receptor function in heart failure.

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