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Blood pressure is the major driving force for plaque formation in aortic-constricted ApoE-/- mice

Maria E Johansson1, Anna Wickman, Ole Skøtt

  • 1Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, Göteborg University, Göteborg, Sweden.

Journal of Hypertension
|September 8, 2006
PubMed
Abstract

Insights

Increased blood pressure, not the renin-angiotensin system (RAS), drives atherosclerosis progression in a mouse model. Blocking the AT1 receptor with losartan did not affect plaque development, suggesting pressure is the primary factor.

Area of Science:

  • Cardiovascular Research
  • Atherosclerosis Studies
  • Renal Physiology

Background:

  • Atherosclerosis is a complex disease influenced by hemodynamic forces and the renin-angiotensin system (RAS).
  • The specific role of increased blood pressure versus RAS activation in driving plaque progression remains debated.
  • Understanding these drivers is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate whether elevated blood pressure or renin-angiotensin system (RAS) activation is the primary driver of atherosclerosis plaque progression.
  • To determine the involvement of AT1 and AT2 receptors in this process using a mouse model.

Main Methods:

  • Aortic constriction (AoC) was induced in male ApoE mice to increase blood pressure.
  • Mice were treated with losartan, a selective AT1 receptor antagonist, or received sham surgery.
  • Plaque area, mean arterial pressure (MAP), and plasma renin concentration (PRC) were measured.

Main Results:

  • Aortic constriction significantly increased mean arterial pressure (MAP) and plasma renin concentration (PRC).
  • Losartan effectively reduced MAP in sham mice but had no effect on MAP in AoC mice.
  • Plaque area significantly increased in AoC mice, but losartan treatment did not alter plaque size or distribution.

Conclusions:

  • Increased blood pressure, not AT1 receptor-mediated RAS activation, appears to be the main driver of atherosclerosis in this aortic constriction model.
  • The study found no evidence for a protective role of the AT2 receptor against atherogenesis in this context.
  • These findings suggest that therapeutic strategies targeting blood pressure may be more effective than AT1 receptor blockade for atherosclerosis in similar conditions.

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