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Updated: May 15, 2026

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
08:41

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues

Published on: June 3, 2019

Impaired vasomotor function induced by the combination of hypertension and hypercholesterolemia

Hizir Kurtel1, Stephen F Rodrigues, Cigdem E Yilmaz

  • 1Department of Physiology, Marmara University School of Medicine, Istanbul, Turkey.

Journal of the American Society of Hypertension : JASH
|January 17, 2013
PubMed

Insights

The combination of hypertension and hypercholesterolemia impairs blood vessel dilation more than either condition alone, involving hydrogen peroxide and blood cells. This impacts endothelial function and vascular reactivity.

Area of Science:

  • Cardiovascular Biology
  • Endothelial Function Research
  • Vascular Physiology

Background:

  • Endothelial dysfunction is a known consequence of hypertension (HTN) and hypercholesterolemia (HCh) individually.
  • The combined effects of HTN and HCh on endothelium-dependent dilation (EDD) and the underlying mechanisms remain less understood.

Purpose of the Study:

  • To investigate the impact of combined HTN and HCh on vasomotor function.
  • To elucidate the mechanisms responsible for altered vascular reactivity in the presence of both HTN and HCh.

Main Methods:

  • Utilized a mouse model with diet-induced hypercholesterolemia and/or hypertension induced by angiotensin II or deoxycorticosterone acetate-salt.
  • Assessed endothelium-dependent and -independent vasomotor responses in aortic vessels.
  • Investigated the role of hydrogen peroxide (H₂O₂) and angiotensin II type 1a receptor (AT1r) signaling.

Main Results:

  • Combined HTN and HCh impaired EDD more significantly than either risk factor alone.
  • Vascular H₂O₂ production was elevated by each risk factor, with a greater increase observed in the combined HTN+HCh group.
  • Impaired EDD was not seen in AT1r-deficient mice, but AT1r-deficient bone marrow chimeras showed more severe impairment.

Conclusions:

  • HTN+HCh does not have an additive effect on vasomotor dysfunction compared to individual risk factors.
  • Both H₂O₂ and blood cell-associated AT1r play crucial roles in the impaired EDD observed in mice with combined HTN and HCh.

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