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En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
Published on: February 25, 2016
Steady endothelial nitric oxide synthase expression in heart failure
Pierre V Ennezat1, Eric Van Belle, Philippe Asseman
1Department of Medicine, Division of Cardiology, Albert Einstein College of Medicine, Bronx, New York, USA. ennezat@yahoo.com
Acta Cardiologica
|July 5, 2007
Summary
Chronic heart failure (CHF) patients do not show reduced endothelial NO synthase (eNOS) gene expression in skeletal muscle. This finding suggests vascular dysfunction in severe heart failure is not due to decreased eNOS expression.
Area of Science:
- Cardiovascular Physiology
- Molecular Biology
- Vascular Biology
Background:
- Reduced nitric oxide (NO)-mediated vasodilation in chronic heart failure (CHF) limb vasculature.
- Previous studies indicated depressed vascular endothelial NO synthase (eNOS) gene expression in experimental heart failure models.
Purpose of the Study:
- To investigate endothelial NO synthase (eNOS) mRNA expression in skeletal muscle vasculature of CHF patients and healthy controls.
Main Methods:
- Quantified eNOS mRNA expression in skeletal muscle samples from 20 CHF patients and 7 healthy subjects.
- Normalized eNOS transcript levels to von Willebrand factor and GAPDH mRNA expression.
Main Results:
- CHF was not associated with a decrease in eNOS expression in skeletal muscle vasculature.
- A trend towards increased eNOS expression was observed in NYHA class IV patients.
Conclusions:
- The observed vascular endothelial dysfunction in severe heart failure is not linked to a specific decrease in endothelial NO synthase gene expression.
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