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Plasma nitroso compounds are decreased in patients with endothelial dysfunction
Christian Heiss1, Thomas Lauer, André Dejam
1Department of Cardiology, Pneumology, and Vascular Medicine, RWTH Aachen, Aachen, Germany.
Journal of the American College of Cardiology
|February 7, 2006
Summary
Plasma nitros(yl)ated species (RXNOs) are depleted in individuals with cardiovascular risk factors and endothelial dysfunction. Lower RXNO levels correlate with impaired vascular function, suggesting a diagnostic role for RXNOs.
Area of Science:
- Cardiovascular Science
- Biochemistry
- Physiology
Background:
- Nitric oxide (NO) plays a systemic role via circulating nitros(yl)ated species (RXNOs).
- RXNOs deliver NO to areas with impaired production, impacting systemic bioactivity.
- Endothelial dysfunction is a key factor in cardiovascular disease development.
Purpose of the Study:
- To investigate the depletion of plasma RXNOs in individuals with cardiovascular risk factors.
- To assess the relationship between RXNO levels and endothelial dysfunction.
- To determine if RXNOs can serve as diagnostic markers for NO bioavailability.
Main Methods:
- Assessed endothelial function using flow-mediated dilation (FMD) in 68 patients with cardiovascular risk factors and 39 controls.
- Measured plasma RXNO concentrations using reductive gas phase chemiluminescence.
- Utilized high-resolution ultrasound for FMD assessment.
Main Results:
- A progressive decrease in FMD was observed with increasing cardiovascular risk factors.
- Plasma RXNO levels significantly decreased with increasing numbers of risk factors (p < 0.01).
- RXNO levels were independently predictive of endothelial function in a multivariate regression model (r = 0.41, p < 0.001).
Conclusions:
- Endothelial dysfunction in patients with cardiovascular risk factors is linked to reduced circulating RXNO levels.
- Plasma RXNOs may serve as valuable diagnostic markers for NO bioavailability and endothelial function.
- Further research is needed to understand the mechanisms behind RXNO decrease and its role in arteriosclerosis.