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Obesity increases prostanoid-mediated vasoconstriction and vascular thromboxane receptor gene expression
Tobias Traupe1, Matthias Lang, Winfried Goettsch
1Medical Policlinic and Clinical Atherosclerosis Research Laboratory, Department of Internal Medicine, University Hospital Zürich, Zürich, Switzerland.
Journal of Hypertension
|November 1, 2002
Summary
Obesity enhances prostanoid-mediated vasoconstriction and increases thromboxane receptor gene expression in blood vessels. These changes contribute to vascular disease, hypertension, and thrombosis linked to obesity.
Area of Science:
- Vascular Biology
- Obesity Research
- Cardiovascular Physiology
Background:
- Vasoconstrictor prostanoids play a role in abnormal vasomotion.
- Atherosclerosis and hypertension are linked to abnormal vascular function.
Purpose of the Study:
- To investigate the impact of obesity on vascular function.
- To examine the expression of genes related to prostanoid action in obese mice.
Main Methods:
- Utilized lean and diet-induced obese mouse models.
- Assessed vascular function via endothelium-dependent contractions.
- Analyzed gene expression using real-time quantitative polymerase chain reaction.
Main Results:
- Obesity increased endothelium-dependent contractions to acetylcholine in carotid arteries.
- Prostanoid-mediated vasoconstriction was observed in the aorta of obese mice.
- Obesity led to a significant upregulation of thromboxane receptor gene expression in carotid arteries.
Conclusions:
- Obesity augments prostanoid-dependent vasoconstriction.
- Increased vascular thromboxane receptor gene expression in obesity promotes vascular disease, hypertension, and thrombosis.