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En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
Published on: February 25, 2016
[Relations between endothelial nitric oxide synthase and angiotensin-converting gene polymorphisms and certain
Władysława Kolasińska-Kloch1, Agata Jabrocka, Beata Kieć-Wilk
1II Klinika Kardiologii Instytutu Kardiologii, Collegium Medicum, Uniwersytetu Jagiellońskiego w Krakowie.
Insights
Cardiological syndrome X (CSX) is linked to metabolic issues like impaired free fatty acid utilization. Genetic variations in eNOS influence nitric oxide (NOx) levels in CSX patients, suggesting a role in endothelial dysfunction.
Area of Science:
- Cardiology
- Genetics
- Biochemistry
Context:
- Cardiological Syndrome X (CSX) presents as effort angina without coronary artery stenosis.
- Genetic predispositions and metabolic disturbances are implicated in CSX development.
- Understanding the biochemical and genetic factors is crucial for CSX pathogenesis.
Purpose:
- To investigate associations between biochemical parameters and ACE/eNOS gene polymorphisms in CSX patients.
- To explore the role of specific eNOS genotypes (VNTR and Glu298Asp) in CSX.
- To identify metabolic disturbances contributing to endothelial injury in CSX.
Summary:
- CSX patients exhibited lower fasting NOx levels, higher post-glucose insulin, and elevated triglycerides/free fatty acids during oral lipid tests.
- eNOS genotypes T/T Glu298Asp and 4/4 VNTR were associated with significantly lower NOx levels.
- Disturbances in free fatty acid utilization are key in CSX-related endothelial injury.
Impact:
- Identifies specific biochemical markers and genetic factors associated with CSX.
- Highlights the role of impaired free fatty acid metabolism and endothelial dysfunction in CSX.
- Provides insights for potential diagnostic or therapeutic targets in managing CSX.
Abstract:
Cardiological syndrome X (CSX) is defined as effort anginal pain, positive exercise tolerance test and absence of angiographically documented stenosis in coronary arteries. Some genetic predispositions and metabolic disturbances can participate in development of this syndrome. The aim of our study was to investigate the associations between some biochemical parameters and polymorphism of ACE and eNOS (VNTR and Glu298Asp) genes in patients with CSX. 36 patients with CSX and a control group of 30 healthy volunteers were included in the study. The genotypes were determined by the polymerase chain reaction. Our study revealed that patients with CSX exerted lower fasting NOx levels, tended to have higher insulin values measured at 1 h of oral glucose tolerance test and higher levels of triglycerides and free fatty acids during oral lipid tolerance test. Patients with genotype T/T Glu298Asp of eNOS and 4/4 VNTR of eNOS revealed lower levels of NOx compared to patients with genotypes G/G and 5/5, respectively (30.5 +/- 7.2 vs 13.2 +/- 4.5; 28.6 +/- 8.4 vs 14.2 +/- 7.4; p<0.05). Thus, we conclude that disturbances in free fatty acid utilization, estimated by postprandial lipaemic test play important roles in the development of endothelial injury in CSX.
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