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Updated: Jun 12, 2026
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A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
Published on: December 2, 2016
Involvement of angiotensin II in the remodeling induced by a chronic decrease in blood flow in rat mesenteric
Céline Baron-Menguy1, Bertrand Toutain, Maud Cousin
1INSERM U771, Angers, France.
Summary
Blood flow reduction causes inward remodeling in arteries, driven by angiotensin II and ERK1/2 activation, not superoxide. Treatments blocking these pathways prevent this vascular remodeling.
Area of Science:
- Vascular biology
- Cardiovascular research
- Physiology
Background:
- Blood flow reduction triggers resistance artery (RA) inward remodeling, implicated in vascular diseases.
- The specific role of flow reduction, independent of pressure or metabolic factors, on RA remodeling remains unclear.
- Angiotensin II is known to influence RA responses to flow, suggesting its potential role in flow-induced remodeling.
Purpose of the Study:
- To investigate the role of angiotensin II in inward remodeling of rat mesenteric RAs due to chronic blood flow reduction.
- To determine if angiotensin I-converting enzyme inhibition or angiotensin II receptor blockade can prevent flow-induced RA remodeling.
- To elucidate the involvement of superoxide production and extracellular signal-regulated kinases 1/2 (ERK1/2) in this remodeling process.
Main Methods:
- In vivo study in rats with experimentally induced low flow (LF) in mesenteric RAs.
- Administration of angiotensin I-converting enzyme inhibitor (perindopril) and angiotensin II type 1 receptor blocker (candesartan).
- Assessment of arterial diameter, endothelium-dependent relaxation, eNOS expression, superoxide production, and ERK1/2 phosphorylation.
Main Results:
- Low flow induced RA diameter reduction, decreased endothelium-dependent relaxation, and lower eNOS expression.
- Increased superoxide production and ERK1/2 phosphorylation were observed in LF arteries.
- Perindopril and candesartan prevented inward remodeling, reduced angiotensin II-induced contractility, and inhibited ERK1/2 activation.
- Inhibition of ERK1/2 also prevented LF-induced diameter reduction.
Conclusions:
- Inward remodeling of mesenteric RAs due to blood flow reduction is dependent on angiotensin II-mediated contraction and ERK1/2 activation.
- This remodeling process occurs independently of superoxide production.
- Findings suggest potential therapeutic targets for vascular disorders characterized by altered blood flow.
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