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Effects of L-arginine on endothelial and cardiac function in rats with heart failure

Q Feng1, A J Fortin, X Lu

  • 1London Health Sciences Centre Research Inc., Department of Medicine, University of Western Ontario, Canada. qfeng@julian.uwo.ca

Insights

Chronic oral L-arginine supplementation in rats with heart failure improved blood vessel function at a lower dose. However, this treatment did not enhance overall cardiac performance in the heart failure model.

Area of Science:

  • Cardiovascular Science
  • Pharmacology
  • Physiology

Background:

  • Heart failure is often associated with impaired endothelial function.
  • L-arginine is a crucial substrate for nitric oxide synthesis, vital for vascular health.
  • Reduced plasma L-arginine levels are observed in heart failure conditions.

Purpose of the Study:

  • To investigate the impact of chronic oral L-arginine treatment on endothelial and cardiovascular function in a rat model of heart failure.
  • To determine the dose-dependent effects of L-arginine on vascular reactivity and cardiac performance.

Main Methods:

  • Induction of heart failure in rats via coronary artery ligation.
  • Administration of L-arginine (12.5 or 50 g/l) or placebo in drinking water for 8 weeks.
  • Assessment of plasma L-arginine levels, ex vivo endothelium-dependent relaxation of aortic rings, and in vivo hemodynamic parameters.

Main Results:

  • Plasma L-arginine levels were significantly lower in heart failure rats compared to sham-operated controls.
  • Low-dose (12.5 g/l) L-arginine treatment improved endothelium-dependent relaxation in aortic rings from heart failure rats.
  • Neither low nor high-dose L-arginine treatment significantly improved hemodynamic parameters in heart failure rats.

Conclusions:

  • Chronic oral L-arginine supplementation at 12.5 g/l enhances endothelial function in rats with heart failure.
  • Higher doses of L-arginine did not yield similar improvements in vascular relaxation.
  • L-arginine treatment failed to improve in vivo cardiac function despite improvements in endothelial-dependent relaxation.

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