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Updated: Jun 2, 2026

An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause
06:18

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

Published on: August 13, 2019

Inhibition of renin-angiotensin system reverses endothelial dysfunction and oxidative stress in estrogen deficient

Lai Ming Yung1, Wing Tak Wong, Xiao Yu Tian

  • 1Institute of Vascular Medicine, Li Ka Shing Institute of Health Sciences, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.

Plos One
|April 12, 2011
PubMed
Abstract

Insights

Estrogen deficiency impairs blood vessel function by increasing renin-angiotensin system (RAS) activity and oxidative stress. Blocking the RAS with valsartan or enalapril improves endothelial dysfunction in ovariectomized rats.

Area of Science:

  • Cardiovascular Science
  • Endocrinology
  • Pharmacology

Background:

  • Estrogen deficiency in postmenopausal women elevates cardiovascular risks.
  • The role of the renin-angiotensin system (RAS) in estrogen deficiency-related vascular dysfunction remains unclear.
  • This study investigates RAS up-regulation and oxidative stress in estrogen deficiency-induced endothelial dysfunction.

Purpose of the Study:

  • To determine if increased RAS activity and oxidative stress contribute to endothelial dysfunction in ovariectomized rats.
  • To evaluate the therapeutic potential of RAS inhibition in mitigating these vascular changes.

Main Methods:

  • Ovariectomized (OVX) rats were treated with valsartan or enalapril.
  • Vascular function was assessed via isometric force measurement in isolated aortae.
  • RAS component expression, oxidative stress markers (ROS), and nitric oxide bioavailability were quantified.

Main Results:

  • Ovariectomy increased expression of ACE, AT(1)R, NAD(P)H oxidase, and nitrotyrosine.
  • Angiotensin II and ROS over-production correlated with reduced eNOS phosphorylation and impaired endothelium-dependent relaxations.
  • RAS inhibition by valsartan or enalapril reversed oxidative stress and endothelial dysfunction.

Conclusions:

  • Estrogen deficiency up-regulates the RAS and increases oxidative stress, leading to endothelial dysfunction.
  • RAS blockade demonstrates significant therapeutic benefit for vascular complications in postmenopausal states.

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