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beta-adrenergic blockade in developing heart failure: effects on myocardial inflammatory cytokines, nitric oxide, and

S D Prabhu1, B Chandrasekar, D R Murray

  • 1Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA. sprabhu@louisville.edu

Circulation
|May 3, 2000
PubMed
Abstract

Insights

Beta-blocker metoprolol reduces heart failure symptoms by lowering inflammatory cytokines tumor necrosis factor-alpha and interleukin-1beta. This effect is independent of nitric oxide pathways.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Pharmacology

Background:

  • The role of beta-adrenergic blockade in modulating myocardial inflammatory cytokines and nitric oxide (NO) during heart failure is not fully understood.
  • Adrenergic activation is implicated in the progression of heart failure.

Purpose of the Study:

  • To investigate the effects of metoprolol on left ventricular remodeling, inflammatory cytokine expression (TNF-alpha, IL-1beta, IL-6), and nitric oxide (NO) pathways in a rat model of heart failure.
  • To elucidate the mechanisms underlying the beneficial effects of beta-adrenergic blockade in heart failure.

Main Methods:

  • Rats with myocardial infarction were treated with oral metoprolol or no therapy for 12 weeks.
  • Evaluated left ventricular (LV) remodeling, systolic function via echocardiography, and myocardial expression of TNF-alpha, IL-1beta, and IL-6.
  • Assessed NO synthase (NOS) activity and responsiveness to isoproterenol.

Main Results:

  • Metoprolol treatment attenuated LV dilatation and systolic dysfunction.
  • Myocardial expression of TNF-alpha and IL-1beta (both mRNA and protein) was significantly reduced by metoprolol.
  • Interleukin-6 (IL-6) expression remained high despite metoprolol treatment.
  • Metoprolol preserved isoproterenol responsiveness through NO-independent mechanisms.

Conclusions:

  • Adrenergic activation contributes to increased myocardial TNF-alpha and IL-1beta expression during heart failure development.
  • Beta-adrenergic blockade, exemplified by metoprolol, may exert beneficial effects by reducing TNF-alpha and IL-1beta expression.
  • These beneficial effects appear to be independent of inducible nitric oxide synthase (iNOS) and NO pathways.

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