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Bradykinin improves left ventricular diastolic function under long-term angiotensin-converting enzyme inhibition in

Masanori Fujii1, Atsuyuki Wada, Takayoshi Tsutamoto

  • 1First Department of Internal Medicine, Central Research Laboratory, Shiga University of Medical Science, Tsukinowa, Seta, Otsu, Japan.

Hypertension (Dallas, Tex. : 1979)
|May 23, 2002
PubMed

Insights

Bradykinin, blocked by FR173657, worsens diastolic heart failure despite ACE inhibitors. Blocking bradykinin impairs relaxation and increases collagen, indicating bradykinin is cardioprotective.

Area of Science:

  • Cardiovascular Physiology
  • Pharmacology
  • Heart Failure Pathophysiology

Background:

  • Systolic and diastolic dysfunction are common in heart failure.
  • The role of bradykinin in left ventricular function under long-term ACE inhibitor treatment requires further elucidation.

Purpose of the Study:

  • To evaluate the effects of a bradykinin type 2 receptor antagonist (FR173657) combined with an ACE inhibitor (enalapril) on tachycardia-induced heart failure in dogs.
  • To compare these effects to enalapril treatment alone.

Main Methods:

  • Tachycardia-induced heart failure model in dogs (270 ppm, 22 days).
  • Administration of FR173657 (0.3 mg/kg/day) with enalapril (1 mg/kg/day) versus enalapril alone.
  • Assessment of left ventricular function, histomorphometry, and gene expression.

Main Results:

  • FR173657 significantly increased left ventricular filling pressure and prolonged relaxation time.
  • FR173657 suppressed endothelial NO synthase and sarcoplasmic reticulum Ca(2+)-ATPase mRNA expression.
  • FR173657 upregulated collagen type I and III mRNA and increased cardiac collagen deposits.

Conclusions:

  • Endogenous bradykinin contributes to ACE inhibitor cardioprotective effects, primarily improving diastolic dysfunction.
  • Bradykinin's protective role involves modulating NO release, Ca(2+) handling, and suppressing collagen accumulation.

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