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Updated: Aug 21, 2026

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
Published on: June 3, 2019
Contribution of vasoconstriction to the origin of atherosclerosis: a conceptual study
William H Gutstein1, Cristian A Pérez
1New York Medical College, Department of Pathology, Valhalla, New York, USA. William.Gutstein@mssm.edu
Insights
Vasoconstriction (VC), a factor causing endothelial injury (EI) and dysfunction (ED), plays a key role in atherosclerosis development. Targeting VC pathways may offer novel therapeutic strategies against this disease.
Area of Science:
- Cardiovascular Research
- Vascular Biology
- Atherosclerosis Pathogenesis
Background:
- Endothelial injury (EI) and dysfunction (ED) are central to atherosclerosis onset.
- Vasoconstriction (VC) is an underappreciated cause of EI/ED.
- VC is linked to proatherogenic stimuli and opposed by vasodilatory effects.
Purpose of the Study:
- To review the role of vasoconstriction (VC) in endothelial injury (EI) and dysfunction (ED).
- To explore the association between VC and atherosclerosis development.
- To highlight novel therapeutic strategies targeting VC.
Main Methods:
- Conceptual review of existing research.
- Analysis of the relationship between VC, EI/ED, and atherosclerosis.
- Discussion of molecular mechanisms and therapeutic targets of VC.
Main Results:
- Vasoconstriction (VC) can directly cause endothelial injury (EI) and dysfunction (ED).
- VC is closely associated with known proatherogenic stimuli.
- Vasodilatory effects of antiatherogenic compounds support the link between VC and atherosclerosis.
Conclusions:
- Vasoconstriction (VC) is a significant contributor to endothelial damage and atherosclerosis.
- Understanding the molecular basis of VC reveals potential therapeutic targets.
- Inhibitors of VC may offer novel strategies for preventing atherosclerotic lesion formation.
Abstract:
Research during the past century has clearly shown that endothelial injury (EI) and/or endothelial dysfunction (ED) are among the major events determining the onset of atherosclerosis. Included in the events that may elicit endothelial damage, vasoconstriction (VC) has received relatively little attention. This conceptual review attempts to show that in elastic and conduit arteries, VC is not only capable of producing EI/ED, but is also closely associated with many recognized proatherogenic stimuli. Of related interest is the observation that a number of suspected antiatherogenic stimuli oppose VC by their vasodilatory effects, lending further support to this relationship. In addition, recent developments in the knowledge of the molecular basis of VC (including the role of specific inhibitors) are discussed, and their potential for preventing lesion formation and thus becoming novel therapeutic alternatives against the onset of atherosclerosis are highlighted.
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