Olmesartan and pravastatin additively reduce development of atherosclerosis in APOE*3Leiden transgenic mice

J Hypertens. 2007 Dec;25(12):2454-62. doi: 10.1097/HJH.0b013e3282ef79f7.

Abstract

Aim: This study was designed to investigate the effect of the angiotensin II receptor blocker olmesartan alone, or in combination with standard treatment with a statin, pravastatin, on atherosclerosis development in APOE*3Leiden transgenic mice.

Methods and results: Four groups of 15 mice received an atherogenic diet alone (plasma cholesterol 17.4 +/- 2.7 mmol/l) or supplemented with either 0.008% (w/w) olmesartan (9.3 mg/kg per day) (plasma cholesterol 16.4 +/- 3.9 mmol/l), 0.03% (w/w) pravastatin (35 mg/kg per day) (plasma cholesterol 14.6 +/- 2.6 mmol/l), or the combination of both (plasma cholesterol 14.5 +/- 2.9 mmol/l) for 6 months. Treatment with olmesartan or pravastatin reduced the development of atherosclerosis as compared to the control group (-46 and -39%, respectively). Pravastatin also reduced the severity of the lesions. As compared to control the combination of both treatments almost fully prevented atherosclerosis (-91%, P < 0.001) and strongly reduced lesion number (-69%), lesion severity (-79%), number of macrophages (-89%) and T lymphocytes (-86%) per cross-section. Treatment with olmesartan alone and in combination with pravastatin inhibited the adhesion of monocytes to the vessel wall (-22%; P < 0.05 and -25%; P < 0.01, respectively), and reduced the relative quantity of macrophages in the lesions (-38%; P < 0.05 and -26%; NS, respectively) as compared to control.

Conclusion: Olmesartan reduced atherosclerosis development mainly by decreasing monocyte adhesion and the relative amount of macrophages, whereas pravastatin inhibited the progression of atherosclerosis to more advanced lesions, reflecting different anti-atherosclerotic modes of action of the two drugs. Combination therapy with olmesartan and pravastatin additively reduced atherosclerosis development, resulting in less and less severe lesions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin II Type 1 Receptor Blockers / administration & dosage*
  • Animals
  • Apolipoprotein E3 / genetics*
  • Atherosclerosis / blood
  • Atherosclerosis / genetics
  • Atherosclerosis / pathology
  • Atherosclerosis / prevention & control*
  • Blood Pressure / drug effects
  • Collagen / metabolism
  • Diet, Atherogenic
  • Drug Synergism
  • Female
  • Humans
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / administration & dosage*
  • Imidazoles / administration & dosage*
  • Inflammation / prevention & control
  • Lipids / blood
  • Macrophages / pathology
  • Mice
  • Mice, Transgenic
  • Monocytes / pathology
  • Muscle, Smooth, Vascular / pathology
  • Pravastatin / administration & dosage*
  • Recombinant Proteins / genetics
  • Serum Amyloid A Protein / metabolism
  • T-Lymphocytes / pathology
  • Tetrazoles / administration & dosage*

Substances

  • Angiotensin II Type 1 Receptor Blockers
  • Apolipoprotein E3
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors
  • Imidazoles
  • Lipids
  • Recombinant Proteins
  • Serum Amyloid A Protein
  • Tetrazoles
  • apolipoprotein E3 (Leidein)
  • olmesartan
  • Collagen
  • Pravastatin