Related Experiment Videos
Dietary salt restriction accelerates atherosclerosis in apolipoprotein E-deficient mice
Ognen Ivanovski1, Dorota Szumilak, Thao Nguyen-Khoa
1INSERM Unit 507, Necker Hospital, 161 Rue de Sèvres, 75015 Paris, France. ivanovski@necker.fr
Atherosclerosis
|May 25, 2005
Summary
Low-salt diets accelerated atherosclerosis in mice by increasing lesion formation and total cholesterol. This may be linked to elevated angiotensin II (ANG-II) levels, suggesting potential cardiovascular risks in humans.
Area of Science:
- Cardiovascular Research
- Atherosclerosis Studies
- Dietary Impact on Health
Background:
- Controversy exists regarding salt intake's effect on cardiovascular mortality.
- Low sodium diets may activate the renin-angiotensin and sympathetic nervous systems.
- Apolipoprotein E deficient (apoE(-/-)) mice are a model for atherosclerosis research.
Purpose of the Study:
- To investigate the impact of low dietary salt on atherosclerotic lesion progression.
- To examine the relationship between salt intake, cholesterol, and angiotensin levels.
- To assess the role of angiotensin II in salt-induced atherosclerosis.
Main Methods:
- Fed apoE(-/-) mice low (0.036% NaCl) or regular (0.64% NaCl) salt diets for 16 weeks.
- Measured atherosclerotic plaque area in the aortic root and thoracic aorta.
- Assessed serum lipids, plasma angiotensin II, and urinary protein/creatinine.
Main Results:
- Low salt intake significantly increased atherosclerotic lesion area in the thoracic aorta.
- Low-salt diet led to higher serum total cholesterol and plasma angiotensin II (ANG-II) levels.
- Atherosclerotic lesion area correlated with ANG-II levels in low-salt mice.
Conclusions:
- Dietary salt restriction accelerated atherosclerotic lesion formation in apoE(-/-) mice.
- The mechanism likely involves increased angiotensin II formation.
- Relevance to human cardiovascular disease requires further evaluation.