X-Message-Number: 12086
Date: Wed, 7 Jul 1999 23:59:39 -0700 (PDT)
From: Doug Skrecky <>
Subject: arginine much better than lovastatin

  Boger RH.  Bode-Boger SM.  Brandes RP.  Phivthong-ngam L.  Bohme M.  Nafe R. 
  Mugge A.  Frolich JC.
  Institute of Clinical Pharmacology, Medical School, Hannover, Germany.
  Dietary L-arginine reduces
  the progression of atherosclerosis in cholesterol-fed rabbits: comparison
  with lovastatin.
  Circulation.  96(4):1282-90, 1997 Aug 19.
  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

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