Associations of molecular genetic predictors of arterial hypertension in adults with the development and course of arterial hypotension in premature newborns

Abstract

Purpose. This study aims at assessing the association of the development and clinical course of arterial hypotension in premature newborns, depending on the polymorphism of the genes of predisposition to hypertension.Material and methods. The study design is prospective, controlled, single-center, and non-randomized. Genomic DNA samples were studied in premature newborns (n = 199), as well as a population sample of adults (n = 100). Newborns with arterial hypotension (n = 23) formed the study group, patients without it (n = 100) formed the comparison group. Loci with already known association with the development of arterial hypertension and coronary heart disease were selected for analysis: AGT (rs4762), AGTR1 (rs5186), ACE (Ins\Del), ADRB1 (rs1801253), ADD1 (rs4961), CYP11B2 (rs1799998), eNOS (rs1799983), eNOS (rs1549758), eNOS (rs2070744). The distribution of allele frequencies between the studied groups of individuals was compared.Results. Premature babies are significantly more likely to be carriers of the allele with the AGT gene. In newborns with arterial hypotension, we additionally revealed a more frequent occurrence of dominant alleles of the eNOS gene, and children with the SS genotype of the eNOS gene required longer vasopressor therapy. Conclusion. The carriage of risky alleles of genes predisposing to arterial hypertension, not only does not increase the risk of arterial hypotension in premature newborns, but also may, in the case of carriage of mutant alleles of the eNOS rs1549758 gene, contribute to less prolonged vasopressor therapy.