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

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

Published on: June 3, 2019

Hemodynamic forces in endothelial dysfunction and vascular aging.

Caitlin Collins¹, Ellie Tzima

¹Department of Cell and Molecular Physiology, McAllister Heart Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.

Experimental Gerontology

|October 5, 2010

Summary

This summary is machine-generated.

Aging impairs blood vessel function, reducing nitric oxide (NO) production and increasing cardiovascular disease risk. Understanding how mechanical forces trigger NO release in aging cells could lead to new therapies.

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Last Updated: Jun 8, 2026

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Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research

Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research

Published on: October 22, 2014

Area of Science:

Cardiovascular biology
Mechanobiology
Aging research

Background:

Aging is a primary risk factor for cardiovascular disease (CVD).
Endothelial dysfunction, characterized by reduced nitric oxide (NO) bioavailability, is common in both vascular aging and CVD.
Aging endothelial cells show senescence and increased oxidative stress, contributing to decreased NO production and insensitivity to shear stress.

Purpose of the Study:

To investigate the mechanisms of mechanotransduction in endothelial cells, specifically how fluid shear stress is converted into intracellular signals.
To understand the age-related decline in endothelial cell response to shear stress.

Main Methods:

The study focuses on endothelial cells and their response to fluid shear stress.
Investigates the conversion of mechanical force into biochemical signals within endothelial cells.

Main Results:

Aging is linked to reduced nitric oxide (NO) production and endothelial dysfunction.
Endothelial cells become less sensitive to fluid shear stress with age, a key factor in decreased NO production.
The precise mechanisms linking mechanical shear stress to intracellular signaling in endothelial cells remain largely unknown.

Conclusions:

Understanding endothelial mechanosignaling is crucial for addressing age-related cardiovascular decline.
Elucidating these pathways may offer novel therapeutic targets for cardiovascular diseases associated with aging.