1 ГЕНЕТИКО-БИОХИМИЧЕСКИЕ МАРКЕРЫ АРТЕРИАЛЬНОЙ ГИПЕРТЕНЗИИ У ПОДРОСТКОВ 1 ГБОУ ВПО «Ростовский ГМУ» Минздрава России, 344022, г. Ростов-на-Дону, Россия активности глутатионпероксидазы и угнетением активности остальных глутатионзависимых ферментов. <...> На этом фоне снижение содержания оксида азота приводит к развитию эндотелиальной дисфункции. <...> Mikashinovitch Z.I., Nagornaia G.Yu., Loseva T.D. the genetic biochemicAl mArkers of ArteriAl hypertension in Adolescents The Rostov state medical university of Minzdrav of Russia, 344022 Rostov-on-Don, Russia The article deals with studying of enzyme activity of first and second lines of anti-oxidant defense in adolescents with arterial hypertension and establishing role of genetic component in realization of mechanism of development of this pathology. <...> The detection of genetically mediated risk of development of arterial hypertension and identification of gene-gene dependencies (ACE, AGT, NOS3) was implemented using technique of PCR-RFLP diagnostic (“DNA-technology”, Russia). <...> The genetic analysis identified in main group the following gene-candidates: deletion genotype DD for ACE, polymorphism M235T T->C gene AGT, version 786 C/C gene NOS3. <...> In adolescents with arterial hypertension imbalance of molecular mechanisms of anti-oxidant defense was revealed. <...> This condition is manifested by imbalance in functioning of enzymes of first line of anti-oxidant defense and accumulation of H2O2, increasing of activity of glutathione peroxidase and depressing of activity of the rest of glutathione depending enzymes. <...> Against this background, decreasing of content of nitrogen oxide results in development of endothelial dysfunction. keywords: arterial hypertension; enzyme anti-oxidant defense; nitrogen oxide; gene polymorphism; adolescents. citation: Klinicheskaya Laboratornaya Diagnostika. <...> Артериальная гипертензия (АГ) в настоящее время является самой распространенной кардиоваскулярной патологией. <...> Известно, что дисбаланс в работе ренинангиотензин-альдостероновой системы, сопровождающийся гиДля <...>