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<bold>Objective.</bold> The aim of the present study was to clarify the endothelial function biomarkers and carotid “intima media” thickness (IMT) changes in relation to <italic>GNB3</italic> (rs5443) and <italic>NOS3</italic> (rs2070744) genes polymorphism in the essential arterial hypertension (EAH).
Methods. One-hundred EAH patients (48 – control) participated in the case-control study. Soluble vascular cell adhesion molecule (sVCAM-1), total NO metabolites (NO2–+NO3–), transcriptional activity of <italic>NOS3</italic> gene, endothelium-dependent flow-mediated dilation of the brachial artery (FMD BA), and carotid IMT were studied. <italic>GNB3</italic> (rs5443) and <italic>NOS3</italic> (rs2070744) genotyping was performed by TaqMan probes (CFX96™Real-Time PCR).
Results. The connection of <italic>NOS3</italic> (rs2070744) with decreased total NO metabolites (F=71.11; p&lt;0.001), reduced <italic>NOS3</italic> genes transcription activity (F=8.71; p&lt;0.001) and increased sVCAM-1 (F=6.96; p=0.002), especially in the <italic>C</italic>-allele carriers (particularly in <italic>CC</italic>-genotype patients with lower NO – 16.46% and 40.88%; p&lt;0.001), lowered the transcription activity of NOS3 gene – 46.03% 7 times (p&lt;0.001), and become higher sVCAM-1 – 35.48% and 89.48% (p&lt;0.001), respectively. ANOVA did not confirm the association of <italic>GNB3</italic> (rs5443) gene with endothelial function and carotid IMT. Severe EAH was associated with increased carotid IMT – 50.0% (p&lt;0.001) and 57.14% (p=0.007), wider carotid arteries – 17.36% (p=0.012) and 21.79% (p=0.004), and decreased NOS3 genes transcription activity – 34.54% (p=0.003). Atherosclerotic plaques were unilateral – 24.77% (χ2=5.35; p=0.021) or bilateral – 27.62% (χ2=5.79; p=0.016). IMT---gt---0.9 mm was followed by a higher BP (p&lt;0.001), FMD BA 11.80% decrease with compensatory increase in carotid arteries diameters – 17.38% and 21.99% (p&lt;0.001) and sVCAM-1 by 20.49% (p=0.005).
<bold>Conclusion.</bold> <italic>NOS3</italic> (rs2070744), but not <italic>GNB3</italic> (rs5443), gene associated with the essential arterial hypertension severity relying upon the endothelial function impairment and <italic>NOS3</italic> genes reduced transcription activity.
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Objective. The aim of the present study was to clarify the endothelial function biomarkers and carotid “intima media” thickness (IMT) changes in relation to GNB3 (rs5443) and NOS3 (rs2070744) genes polymorphism in the essential arterial hypertension (EAH).
Methods. One-hundred EAH patients (48 – control) participated in the case-control study. Soluble vascular cell adhesion molecule (sVCAM-1), total NO metabolites (NO2–+NO3–), transcriptional activity of NOS3 gene, endothelium-dependent flow-mediated dilation of the brachial artery (FMD BA), and carotid IMT were studied. GNB3 (rs5443) and NOS3 (rs2070744) genotyping was performed by TaqMan probes (CFX96™Real-Time PCR).
Results. The connection of NOS3 (rs2070744) with decreased total NO metabolites (F=71.11; p<0.001), reduced NOS3 genes transcription activity (F=8.71; p<0.001) and increased sVCAM-1 (F=6.96; p=0.002), especially in the C-allele carriers (particularly in CC-genotype patients with lower NO – 16.46% and 40.88%; p<0.001), lowered the transcription activity of NOS3 gene – 46.03% 7 times (p<0.001), and become higher sVCAM-1 – 35.48% and 89.48% (p<0.001), respectively. ANOVA did not confirm the association of GNB3 (rs5443) gene with endothelial function and carotid IMT. Severe EAH was associated with increased carotid IMT – 50.0% (p<0.001) and 57.14% (p=0.007), wider carotid arteries – 17.36% (p=0.012) and 21.79% (p=0.004), and decreased NOS3 genes transcription activity – 34.54% (p=0.003). Atherosclerotic plaques were unilateral – 24.77% (χ2=5.35; p=0.021) or bilateral – 27.62% (χ2=5.79; p=0.016). IMT---gt---0.9 mm was followed by a higher BP (p<0.001), FMD BA 11.80% decrease with compensatory increase in carotid arteries diameters – 17.38% and 21.99% (p<0.001) and sVCAM-1 by 20.49% (p=0.005).
Conclusion. NOS3 (rs2070744), but not GNB3 (rs5443), gene associated with the essential arterial hypertension severity relying upon the endothelial function impairment and NOS3 genes reduced transcription activity.

Endothelium function biomarkers and carotid intima-media thickness changes in relation to NOS3 (rs2070744) and GNB3 (rs5443) genes polymorphism in the essential arterial hypertension

Endocrine Regulations

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Objective. The aim of the present study was to clarify the endothelial function biomarkers and carotid “intima media” thickness (IMT) changes in relation to...

Endothelium function biomarkers and carotid intima-media thickness changes in relation to NOS3 (rs2070744) and GNB3 (rs5443) genes polymorphism in the essential arterial hypertension

Data publikacji: 30 kwi 2022

Zakres stron: 104 - 114

DOI: https://doi.org/10.2478/enr-2022-0012

Słowa kluczowe
(rs2070744), but not (rs5443), gene associated with the essential arterial hypertension severity relying upon the endothelial function impairment and genes reduced transcription activity

© 2022 Andrii R. Sydorchuk et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Endothelium function biomarkers and carotid intima-media thickness changes in relation to NOS3 (rs2070744) and GNB3 (rs5443) genes polymorphism in the essential arterial hypertension

Data publikacji: 30 kwi 2022

Zakres stron: 104 - 114

DOI: https://doi.org/10.2478/enr-2022-0012

Słowa kluczowe(rs2070744), but not (rs5443), gene associated with the essential arterial hypertension severity relying upon the endothelial function impairment and genes reduced transcription activity

© 2022 Andrii R. Sydorchuk et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Słowa kluczowe
(rs2070744), but not (rs5443), gene associated with the essential arterial hypertension severity relying upon the endothelial function impairment and genes reduced transcription activity