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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">arthyper</journal-id><journal-title-group><journal-title xml:lang="ru">Артериальная гипертензия</journal-title><trans-title-group xml:lang="en"><trans-title>"Arterial’naya Gipertenziya" ("Arterial Hypertension")</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1607-419X</issn><issn pub-type="epub">2411-8524</issn><publisher><publisher-name>Antihypertensive League</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.18705/1607-419X-2007-13-2-119-127</article-id><article-id custom-type="elpub" pub-id-type="custom">arthyper-1115</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ОБЗОР</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEW</subject></subj-group></article-categories><title-group><article-title>Ассиметричный диметиларгинин
в качестве медиатора и маркера развития
эндотелиальной дисфункции</article-title><trans-title-group xml:lang="en"><trans-title>ADMA as a marker and mediator
of endothelial dysfunction progression</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Жлоба</surname><given-names>А. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Zhloba</surname><given-names>A. A.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Отдел биохимии НИЦ СПбГМУ им. И.П. Павлова</institution></aff><aff xml:lang="en"><institution>St.-Petersburg State I.P. Pavlov Medical University</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2007</year></pub-date><pub-date pub-type="epub"><day>28</day><month>04</month><year>2007</year></pub-date><volume>13</volume><issue>2</issue><fpage>119</fpage><lpage>127</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Жлоба А.А., 2007</copyright-statement><copyright-year>2007</copyright-year><copyright-holder xml:lang="ru">Жлоба А.А.</copyright-holder><copyright-holder xml:lang="en">Zhloba A.A.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://htn.almazovcentre.ru/jour/article/view/1115">https://htn.almazovcentre.ru/jour/article/view/1115</self-uri><abstract><p>Нарушение эндотелий - зависимой вазодилятации является одним из основных эффектов, возникающих при накоплении ассиметричного диметиларгинина (АДМА) и гомоцистеина в организме.
Повышенный уровень АДМА в плазме крови может формироваться при умеренной форме гипергомоцистеинемии (ГГци). В большинстве случаев торможение eNOS иод, влиянием гомоцистеина возникает за счет ассиметричного диметиларгинина (АДМА), накапливающегося в эндотелиоцитах. Механизм этого явления, по-видимому, состоит в том, что гомоцистеин в клетке превращается в S-аденозилгомоцистеин - мощный ингибитор диметилар-гинин-диметиламиногидролазы (ДДАГ). Данные литературы указывают на то, что развитие эндотелиальной дисфункции может зависеть как от сочетания всех этих факторов, так и в отсутствие одного из них.</p></abstract><trans-abstract xml:lang="en"><p>Impaired endothelium-dependent vasodilatation is one of a main effects followed from elevation ADMA and homocysteine.
Homocyseine dependent inhibition of the enzymatic function of eNOS arises as associated event under the direct influence of ADMA elevation in endothelial cells. The cellular mechanism of this phenomenon, apparently, consists in transformation of homocysteine in S-adenosyl-homocysteine which inhibits dimethylarginine dimethylamino hydrolase (DDAH). The literature data show up dependence of endothelial vasomotor dysfunction development both from on a combination of these factors, and in case of one lack.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>АДМА</kwd><kwd>гомоцистеин</kwd><kwd>эндотелиальная дисфункция</kwd></kwd-group><kwd-group xml:lang="en"><kwd>ADMA</kwd><kwd>homocysteine</kwd><kwd>endothelial dysfunction</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Gokce, N. L-Arginine and Hypertension//J. 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