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April 7, 2009HypertensionOpen Access

Swimming Prevents Vulnerable Atherosclerotic Plaque Development in Hypertensive 2-Kidney, 1-Clip Mice by Modulating Angiotensin II Type 1 Receptor Expression Independently From Hemodynamic Changes

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Why the study?

Does swimming improve atherosclerotic plaque stabilization in hypertensive Apolipoprotein E(-/-) mice?

Key Points

To evaluate whether regular swimming stabilizes vulnerable atherosclerotic plaques in hypertensive mice and to determine the underlying blood pressure-independent molecular mechanisms.
Assigned Apolipoprotein E-deficient mice with angiotensin II-dependent vulnerable plaques (2-kidney, 1-clip), angiotensin II-independent stable plaques (1-kidney, 1-clip), or normotensive controls to 5 weeks of regular swimming or sedentary housing.
Assessed blood pressure, plaque morphology (fibrous cap thickness, macrophage content, smooth muscle cells), aortic angiotensin II receptor mRNA levels, sympathetic tone, and immune cell populations.
Exercised 2-kidney, 1-clip mice exhibited significantly stabilized plaques—featuring reduced media degeneration, layering, and macrophage infiltration along with increased smooth muscle cells—compared to sedentary controls, despite no change in blood pressure.
Swimming significantly downregulated aortic angiotensin II type 1 receptor mRNA expression and diminished sympathetic tone, without modifying angiotensin II type 2 receptor levels, endothelial function, or T-helper cell balance.

Structured PICO

Does swimming improve atherosclerotic plaque stabilization in hypertensive Apolipoprotein E(-/-) mice?

P

Population

Apolipoprotein E(-/-) mice with vulnerable (2-kidney, 1-clip: angiotensin [Ang] II-dependent hypertension model) or stable atherosclerotic plaques (1-kidney, 1-clip: Ang II-independent hypertension model and normotensive shams)

I

Intervention

Swimming regularly for 5 weeks

C

Comparator

Sedentary controls

O

Outcome

Atherosclerotic plaque stability (fibrous cap thickness, media degeneration, layering, macrophage content, and smooth muscle cells)surrogate

Swimming prevents atherosclerosis progression and plaque vulnerability in a mouse model of Ang II-mediated hypertension, likely by downregulating aortic Ang II type 1 receptor expression independently of hemodynamic changes.

Discussion

No takes yet. Share an insight, caveat, or question.

Implication

These animal data are hypothesis-generating for exercise in Ang II hypertension; should not yet influence clinical practice.

Cite This Study

Pellegrin et al. (2009) studied this question.

synapsesocial.com/papers/6a953f32aa92d0f3572c9b5a https://doi.org/10.1161/hypertensionaha.108.128165

Topics

Hypertension management

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