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Related Experiment Videos

Hypertension and endothelial dysfunction in apolipoprotein E knockout mice.

R Yang1, L Powell-Braxton, A K Ogaoawara

  • 1Department of Cardiovascular Research, Genentech, Inc, South San Francisco, CA 94080, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|November 13, 1999
PubMed
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Atherosclerosis in mice lacking apolipoprotein E (ApoE) leads to hypertension and impaired nitric oxide-mediated vasodilation. Early-stage hypercholesterolemia alone did not cause these issues.

Area of Science:

  • Cardiovascular Science
  • Animal Models of Disease
  • Pharmacology

Background:

  • Mice lacking apolipoprotein E (ApoE) are a model for studying hypercholesterolemia and atherosclerosis.
  • Atherosclerosis progression is associated with hemodynamic changes and endothelial dysfunction.

Purpose of the Study:

  • To investigate hemodynamics and endothelial function in ApoE-deficient mice at different stages of disease.
  • To determine the role of atherosclerosis in hypertension and endothelial dysfunction.

Main Methods:

  • Hemodynamic measurements (arterial pressure, cardiac remodeling) and histopathological analysis of renal arteries were performed in 6-week-old and 7.5-month-old Apoe(-/-) mice and controls.
  • Endothelial function was assessed by measuring cutaneous blood perfusion changes in response to nitric oxide-mediated (mustard oil) and cyclic adenosine monophosphate-mediated (cilostazol) vasodilation.

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Main Results:

  • 7.5-month-old Apoe(-/-) mice exhibited hypertension, cardiac remodeling, renal artery atherosclerosis, and blunted nitric oxide-mediated vasodilation compared to controls.
  • 6-week-old Apoe(-/-) mice, with hypercholesterolemia but no atherosclerosis, showed normal hemodynamics and endothelial function.
  • Cilostazol-induced vasodilation was preserved in 7.5-month-old Apoe(-/-) mice, suggesting specific impairment of nitric oxide pathways.

Conclusions:

  • Hypertension and endothelial dysfunction in advanced ApoE-deficient atherosclerosis are primarily driven by the atherosclerotic process.
  • Nitric oxide-mediated vasodilation is compromised in the presence of significant atherosclerosis.
  • Early hypercholesterolemia alone does not induce significant hypertension or endothelial dysfunction in this model.