Pearson and Shaw might have been right about arginine

From: Doug Skrecky (oberon@vcn.bc.ca)
Date: Sat Nov 06 1999 - 22:18:56 MST


Authors
  Boger RH. Bode-Boger SM. Brandes RP. Phivthong-ngam L. Bohme M. Nafe R.
  Mugge A. Frolich JC.
Institution
  Institute of Clinical Pharmacology, Medical School, Hannover, Germany.
Title
  Dietary L-arginine reduces
  the progression of
  atherosclerosis in cholesterol-fed rabbits: comparison with
  lovastatin.
Source
  Circulation. 96(4):1282-90, 1997 Aug 19.
Abstract
  BACKGROUND: We investigated whether
  L-arginine induces regression of preexisting
  atheromatous lesions and reversal of
  endothelial dysfunction in hypercholesterolemic rabbits,
  whether similar effects can be obtained by
  cholesterol-lowering therapy with lovastatin, and which
  mechanism leads to these effects. METHODS AND RESULTS:
  Rabbits were fed 1% cholesterol for 4 weeks and 0.5% cholesterol for an
  additional 12 weeks. Two groups of cholesterol-fed rabbits were treated with
  L-arginine (2.0% in drinking water) or lovastatin (10 mg/d)
  during weeks 5 through 16. Systemic nitric oxide (NO) formation was assessed
  as the urinary excretion rates of nitrate and cGMP in weekly
  intervals. Cholesterol feeding progressively reduced urinary nitrate
  excretion to approximately 40% of baseline (P<.05) and increased plasma
  concentrations of asymmetrical dimethylarginine (ADMA), an endogenous NO
  synthesis inhibitor. Dietary
  L-arginine reversed the reduction in plasma
  L-arginine/ADMA ratio and partly restored urinary excretion
  of nitrate and cGMP (each P<.05 vs cholesterol) but did not change plasma
  cholesterol levels. L-Arginine completely blocked
  the progression of carotid intimal plaques,
  reduced aortic intimal thickening, and preserved
  endothelium-dependent vasodilator function. Lovastatin
  treatment reduced plasma cholesterol by 32% but did not improve urinary
  nitrate or cGMP excretion or endothelium-dependent
  vasodilation. Lovastatin had a weaker inhibitory effect on carotid plaque
  formation and aortic intimal thickening than L-arginine.
  L-Arginine inhibited but lovastatin potentiated superoxide
  radical generation in the atherosclerotic
  vascular wall. CONCLUSIONS: Dietary
  L-arginine improves NO-dependent vasodilator function in
  cholesterol-fed rabbits and completely blocks the
  progression of plaques via restoration of NO synthase
  substrate availability and reduction of vascular oxidative stress. Lovastatin
  treatment has a weaker inhibitory effect on the
  progression of atherosclerosis and no
  effect on vascular NO elaboration, which may be due to its stimulatory effect
  on vascular superoxide radical generation.



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