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Updated: May 15, 2026

An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause

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Sildenafil restores endothelial function in the apolipoprotein E knockout mouse.

Camille M Balarini¹, Marcos A Leal, Isabele B S Gomes

¹Dept, of Physiological Sciences, Health Sciences Center, Federal University of Espirito Santo, Vitoria, ES, Brazil.

Journal of Translational Medicine

|January 8, 2013

Summary

This summary is machine-generated.

Sildenafil treatment improved endothelial function and reduced atherosclerosis in mice by enhancing nitric oxide (NO) pathways and decreasing oxidative stress. This study shows potential cardiovascular benefits of sildenafil beyond erectile dysfunction.

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Published on: August 25, 2020

Area of Science:

Cardiovascular Research
Pharmacology
Molecular Biology

Background:

Atherosclerosis is an inflammatory arterial disease driven by endothelial dysfunction and an imbalance of reactive oxygen species (ROS) and nitric oxide (NO).
Sildenafil, a phosphodiesterase-5 (PDE5) inhibitor, enhances NO effects and is used for erectile dysfunction.

Purpose of the Study:

To investigate the effects of sildenafil on endothelial function and atherosclerosis progression.
To evaluate sildenafil's impact in apolipoprotein E knockout (apoE-/-) mice, a model of spontaneous hypercholesterolemia.

Main Methods:

ApoE-/- mice were treated with sildenafil (40 mg/kg/day for 3 weeks) and compared to untreated apoE-/- and wild-type (WT) mice.
Aortic ring relaxation responses to acetylcholine (ACh) were assessed, with roles of NO and ROS investigated using L-NAME and apocynin inhibitors.
Atherosclerotic lesion quantification and superoxide production were evaluated.

Main Results:

Sildenafil restored acetylcholine-induced vasodilation in apoE-/- mice.
Nitric oxide (NO) played an augmented role in vasodilation in sildenafil-treated mice, while reactive oxygen species (ROS) levels were reduced.
Sildenafil treatment led to a significant ~40% reduction in aortic plaque deposition.

Conclusions:

This study demonstrates the beneficial effects of chronic sildenafil treatment on endothelial dysfunction and atherosclerosis in a mouse model.
Sildenafil's positive impact on endothelial function is primarily mediated by enhancing the NO pathway and reducing oxidative stress.