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Updated: May 11, 2026

Chemiluminescence-based Assays for Detection of Nitric Oxide and its Derivatives from Autoxidation and Nitrosated Compounds
Published on: February 16, 2022
Genetic influence on the relation between exhaled nitric oxide and pulse wave reflection
David Laszlo Tarnoki1, Adam Domonkos Tarnoki, Emanuela Medda
1Department of Radiology and Oncotherapy, Semmelweis University, Budapest, Hungary, 78/a Ulloi Street, Budapest 1082, Hungary. tarnoki4@gmail.com
Genetic factors significantly influence fractional exhaled nitric oxide (FE(NO)) levels and arterial elasticity, with shared genes linking FE(NO) and aortic augmentation index (Aix(ao)). Environmental factors also play a role in FE(NO) variation.
Area of Science:
- Genetics and Genomics
- Cardiovascular Physiology
- Respiratory Medicine
Background:
- Nitric oxide is crucial for airway and blood vessel development.
- Fractional exhaled nitric oxide (FE(NO)) is inversely associated with atherosclerosis risk factors.
- Understanding genetic and environmental influences on FE(NO) and arterial elasticity is important for disease research.
Purpose of the Study:
- To determine the heritability of FE(NO) and arterial elasticity (aortic augmentation index, Aix(ao)).
- To investigate the genetic and environmental contributions to variations in FE(NO) and Aix(ao).
- To examine the genetic and environmental covariation between FE(NO) and Aix(ao).
Main Methods:
- Adult Caucasian twin pairs (n=117) were recruited across three countries.
- FE(NO) was measured using an electrochemical sensor.
- Arterial elasticity (Aix(ao)) was assessed via oscillometric pulse wave analysis.
- Bivariate Cholesky decomposition was employed to analyze genetic and environmental influences.
Main Results:
- Genetic factors accounted for 58% of the variation in FE(NO).
- Non-shared environmental influences explained the remaining 42% of FE(NO) variation.
- A significant negative genetic correlation was found between FE(NO) and Aix(ao) (r(g) = -0.25).
- Covariance between FE(NO) and Aix(ao) is attributed entirely to shared genetic factors.
Conclusions:
- Variations in human FE(NO) are influenced by both genetic and non-shared environmental effects.
- Shared genetic factors underlie the covariance between FE(NO) and arterial elasticity.
- These findings suggest a genetic overlap relevant to cardiovascular and respiratory diseases, warranting further genetic studies.
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