The lipid profile depends on the endothelial NO synthase gene promoter T786C-polymorphism in patients with arterial hypertension

Roman Hnizdyukh; Svitlana Pidruchna; Volodymyr Shmanko; Petro Lykhatskyi; Liliya Palytsia; Iryna Zavarynska; Nataliya Tkachuk; Oleksandr Tokarskyy

Roman Hnizdyukh Department of Pharmacology and Clinical Pharmacology, Ternopil National Medical University, Ternopil, Ukraine
Svitlana Pidruchna Department of Medical Biochemistry, Ternopil National Medical University, Ternopil, Ukraine
Volodymyr Shmanko Department of Pharmacology and Clinical Pharmacology, Ternopil National Medical University, Ternopil, Ukraine
Petro Lykhatskyi Department of Medical Biochemistry, Ternopil National Medical University, Ternopil, Ukraine
Liliya Palytsia Department of Medical Biochemistry, Ternopil National Medical University, Ternopil, Ukraine
Iryna Zavarynska Department of Ukrainian Language and and Slavic Studies, Ternopil National Pedagogical University, Ternopil, Ukraine
Nataliya Tkachuk Department of Microbiology, Virology, and Immunology, Ternopil National Medical University, Ternopil, Ukraine
Oleksandr Tokarskyy Department of Medical Biochemistry, Ternopil National Medical University, Ternopil, Ukraine

Keywords: gene polymorphism T786C, endothelial NO-synthase gene promoter, arterial hypertension, dyslipidemia

Abstract

According to the research data from recent years, genetic factors play an important role in the development and course of arterial hypertension (AHT). The study of the T786C polymorphism of the endothelial NO-synthase (NOS3) gene promoter in the case of arterial hypertension is a promising direction for determining the relationship between heredity, arterial hypertension, and dyslipidemia. A number of 86 AHT patients participated in the experiment, while the control group consisted of 30 practically healthy people. Indicators of lipid metabolism in the blood serum were determined. The T786C promoter of the endothelial NO-synthase (NOS3) gene was analyzed using the PCR method with electrophoretic detection of the results. The level of HDL, as an antiatherogenic factor, in the group of NOS3 gene “CC” genotype carriers was significantly lower by 45.8% than the HDL level of the “TT” genotype carriers, 0.58±0.06 vs. 1.07±0.03 mmol/L, respectively. A decrease in the HDL at the expense of an increase in the LDL and VLDL in AHT patients contributes to the formation of a secondary type IV dyslipidemia. “CC” genotype eNOS gene patients had a more pronounced disturbance of the lipid profile compared to patients with the “TT” and “TC” genotypes. Therefore, the “CC” genotype of the eNOS3 gene promoter may predict the development of dyslipidemia in patients with arterial hypertension and additional cardiovascular risk factors for the development of hypertension in patients.