Abstract
Arterial hypertension (AH) is one of the most serious problems of modern health care. In the northern regions it has become a catastrophe, being the most common cause of early disability and mortality among the employable newly-arrived population. At high latitudes, AH is characterized by a more severe course; it is accompanied by early damage to target organs; and it is more often in young people. AH occurs as a result of a combined interaction of polymorphism in genes, which are involved in blood pressure regulation. It is also provoked by the environmental factors. 
 The aim of the study is to assess the prevalence of polymorphisms in four AH candidate genes (AGT (rs4762), AGTR1 (rs5186), ADD1 (rs4961), NOS3 (rs2070744)) in the newly arrived population of the North-East Russia.
 Materials and methods. The cross-sectional study involved practically healthy unrelated men, mostly Europeans, living or born on the territory of the Magadan region (n=101). The average age of the subjects was 46.12±1.5 (20–77 years old). PCR was used to perform molecular genetic testing of genes directly involved in the work of the main blood pressure regulation systems: AGT, AGTR1, ADD1, NOS3. The author calculated phenotypic and gene frequencies, observed and expected heterozygosity levels, Wright's fixation index (D) and population genetic distance (according to Nei). Clustering methods and multidimensional scaling were used to visualize the genetic relationship of different populations.
 Results. In the newly arrived population of the North-East Russia, genotype distribution corresponds to the Hardy – Weinberg equilibrium (p>0.05). Allelic diversity for the studied loci varies from Ho=0.25 (AGT locus) to Ho=0.44 (eNOS locus).
 Conclusion. The result of the study is the revealed characteristics of AH candidate gene frequency in the newly arrived population of the North-East Russia. It is found that allelic variants that increase the risk of AH developing are minor. Their frequency varies from 13.37 % (AGT*T allele, AGT locus) to 35.64 % (eNOS*C allele, eNOS locus).
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