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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">cardiovascular</journal-id><journal-title-group><journal-title xml:lang="ru">Кардиоваскулярная терапия и профилактика</journal-title><trans-title-group xml:lang="en"><trans-title>Cardiovascular Therapy and Prevention</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1728-8800</issn><issn pub-type="epub">2619-0125</issn><publisher><publisher-name>«SILICEA-POLIGRAF» LLC</publisher-name></publisher></journal-meta><article-meta><article-id custom-type="elpub" pub-id-type="custom">cardiovascular-2140</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>АРТЕРИАЛЬНАЯ ГИПЕРТОНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ARTERIAL HYPERTENSION</subject></subj-group></article-categories><title-group><article-title>Обратное развитие сосудистой гипертрофии под действием блокады рецепторов ангиотензина II у пациентов с артериальной гипертензией</article-title><trans-title-group xml:lang="en"><trans-title>Reversal of vascular hypertrophy in hypertensive patients through blockade of angiotensin II receptors</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>Смит</surname><given-names>Р. Д.</given-names></name><name name-style="western" xml:lang="en"><surname>Smith</surname><given-names>R. D.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Yokoyama</surname><given-names>H.</given-names></name><name name-style="western" xml:lang="en"><surname>Yokoyamaa</surname><given-names>H.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Averill</surname><given-names>D. B.</given-names></name><name name-style="western" xml:lang="en"><surname>Averill</surname><given-names>D. B.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Schiffrin</surname><given-names>E. L.</given-names></name><name name-style="western" xml:lang="en"><surname>Schiffrin</surname><given-names>E. L.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Department of Medicine</p></bio><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Ferrario</surname><given-names>C. M.</given-names></name><name name-style="western" xml:lang="en"><surname>Ferrario</surname><given-names>C. M.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina</institution><country>Соединённые Штаты Америки</country></aff><aff xml:lang="en"><institution>Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina</institution><country>United States</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Sir Mortimer B. Davis Jewish General Hospital, McGill University, Montreal, Quebec</institution><country>Канада</country></aff><aff xml:lang="en"><institution>Department of Medicine, Sir Mortimer B. Davis Jewish General Hospital, McGill University, Montreal, Quebec</institution><country>Canada</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2010</year></pub-date><pub-date pub-type="epub"><day>20</day><month>12</month><year>2010</year></pub-date><volume>9</volume><issue>6</issue><fpage>17</fpage><lpage>24</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Смит Р.Д., Yokoyama H., Averill D.B., Schiffrin E.L., Ferrario C.M., 2010</copyright-statement><copyright-year>2010</copyright-year><copyright-holder xml:lang="ru">Смит Р.Д., Yokoyama H., Averill D.B., Schiffrin E.L., Ferrario C.M.</copyright-holder><copyright-holder xml:lang="en">Smith R.D., Yokoyamaa H., Averill D.B., Schiffrin E.L., Ferrario C.M.</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://cardiovascular.elpub.ru/jour/article/view/2140">https://cardiovascular.elpub.ru/jour/article/view/2140</self-uri><abstract><p>Цель. Определить, способна ли терапия блокаторами рецепторов ангиотензина (БРА) вызвать обратное развитие гипертрофии стенок сосудов, независимо от степени снижения артериального давления (АД). Материал и методы. В исследовании пациенты с артериальной гипертензией (АГ) I ст. и без сопутствующего сахарного диабета — 61 % мужчин; возраст 38-67 лет, после 4-недельного периода отмывания, рандомизировались в группы (гр.) олмесартана медоксомила (20-40 мг/сут.) либо атенолола (50-100 мг/ сут.). Дополнительная антигипертензивная терапия (АГТ) включала гидрохлортиазид, амлодипин либо гидралазин. Целевой уровень АД &lt;140/90 мм рт.ст. Исходно и через 1 год от начала терапии оценивали процесс ремоделирования сосудов, путем миографического исследования подкожных резистивных артерий глютеальной области. Биоптаты были получены у 22 больных из гр. атенолола, 27 пациентов из гр. олмесартана медоксомила и 11 здоровых лиц из гр. контроля (ГК). Результаты. Степень снижения АД, по сравнению с исходным уровнем, была сопоставимой на фоне приема олмесартана медоксомила — со 149±11/92±8 до 120±9/77±6 мм рт.ст. (р&lt;0,05); и атенолола — со 147±10/90±6 до 125±12/78±7 мм рт.ст. (р&lt;0,05). Через 40 нед. терапии величина р для сравнения двух гр. составляла 0,08. Через 1 год лечения отношение толщины сосудистой стенки к диаметру просвета сосуда достоверно снизилось в гр. олмесартана медоксомила с 14,9 % до 11,1 % (р&lt;0,01), в то время как на фоне приема атенолола этот показатель существенно не изменился — 16,0 % и 15,5 % (нд). В ГК величина отношения толщины сосудистой стенки к диаметру просвета сосуда составляла 11,0 %. Заключение. У больных с эссенциальной АГ прием БРА сопровождался обратным развитием гипертрофии стенок резистивных сосудов, с достижением показателей, сходных с таковыми у здоровых, нормотензивных лиц. Этот положительный эффект не зависел от степени снижения уровня АД.</p></abstract><trans-abstract xml:lang="en"><p>Aim. May blockade of the angiotensin II type 1 receptor (AT1) with an angiotensin receptor blocker reverse vascular pathology independent of blood pressure (BP) lowering. Material and methods. Stage I hypertensive, nondiabetic patients (61% male; age 38 to 67 years) were randomized after a 4-week washout period to olmesartan medoxomil 20 to 40 mg or atenolol 50 to 100 mg plus additional agents (hydrochlorothiazide, amlodipine, or hydralazine) as needed for a goal BP &lt;140/90 mm Hg. At baseline and after 1 year of treatment, subcutaneous gluteal resistance arteries were examined on a pressurized myograph to evaluate remodeling. Biopsies were available from 22 atenolol recipients, 27 olmesartan medoxomil recipients, and 11 normal volunteer controls. Results. BP was reduced to a comparable degree by olmesartan medoxomil (from 149±11/92±8 mm Hg to 120±9/77±6 mm Hg; p&lt;0,05 [mean ± standard deviation]) and atenolol (from 147±10/90±6 mm Hg to 125±12/78±7 mm Hg; p&lt;0,05 [mean ± standard deviation]) from baseline for each arm (p=0,08 for the 40-week treatment mean between arms). After one year’s treatment, the wall-to-lumen ratio in arteries from patients treated with olmesartan medoxomil was significantly reduced (from 14,9% to 11,1%; p&lt;0,01), whereas no significant change was observed in arteries from atenolol-treated patients (from 16,0% to 15,5%; p=NS); the wall- to-lumen ratio in controls was 11,0%. Conclusion. Blockade of AT1 receptors showed a superior corrective effect on the altered structure of resistance arteries in essential hypertension that was independent of the magnitude of BP reduction, and resulted in values similar to those in normotensive controls.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>ангиотензин II</kwd><kwd>атенолол</kwd><kwd>артериальное давление</kwd><kwd>артериальная гипертензия</kwd><kwd>олмесартан</kwd></kwd-group><kwd-group xml:lang="en"><kwd>angiotensin II</kwd><kwd>atenolol</kwd><kwd>blood pressure</kwd><kwd>arterial hypertension</kwd><kwd>olmesartan</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">Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 Report. 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