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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">nefr</journal-id><journal-title-group><journal-title xml:lang="ru">Нефрология</journal-title><trans-title-group xml:lang="en"><trans-title>Nephrology (Saint-Petersburg)</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1561-6274</issn><issn pub-type="epub">2541-9439</issn><publisher><publisher-name>Pavlov First Saint-Petersburg State Medical University</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.36485/1561-6274-2024-28-1-105-115</article-id><article-id custom-type="edn" pub-id-type="custom">SMKCYB</article-id><article-id custom-type="elpub" pub-id-type="custom">nefr-2296</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>ОРИГИНАЛЬНЫЕ СТАТЬИ. ЭКСПЕРИМЕНТАЛЬНЫЕ ИССЛЕДОВАНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ORIGINAL ARTICLES. EXPERIMENTAL INVESTIGATION</subject></subj-group></article-categories><title-group><article-title>Влияние избыточного потребления соли на функциональное состояние сосудов микроциркуляторного русла кожи у крыс с дисфункцией почек</article-title><trans-title-group xml:lang="en"><trans-title>Influence of excessive salt consumption on the functional state of microvascular vessels of the skin of rats with renal dysfunction</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-0188-5173</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Иванова</surname><given-names>Г. Т.</given-names></name><name name-style="western" xml:lang="en"><surname>Ivanova</surname><given-names>G. T.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Иванова Галина Тажимовна - ведущий научный сотрудник, канд. биол. наук, лаборатория физиологии сердечно-сосудистой и лимфатической систем,</p><p>199034, Санкт-Петербург, наб. Макарова, д. 6</p></bio><bio xml:lang="en"><p>Ivanova Galina T. - Leading researcher, PhD. Biol. sciences, Laboratory of Physiology of Cardiovascular and Lymphatic Systems,</p><p>199034, St. Petersburg, nab. Makarova, D. 6</p></bio><email xlink:type="simple">ivanovagt@infran.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-5722-8693</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Хасун</surname><given-names>М. Х.</given-names></name><name name-style="western" xml:lang="en"><surname>Khasun</surname><given-names>M. H.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Хасун Мохамад Халедович - доц., канд. мед. наук, кафедра пропедевтики внутренних болезней,</p><p>197022, Санкт-Петербург, ул. Л. Толстого, д. 17, корп. 54</p></bio><bio xml:lang="en"><p>Khasun Mohamad H. - MD, PhD, Associate Professor, Department of Propaedeutics of Internal Diseases,</p><p>197022, St. Petersburg, L. Tolstogo str., 17, building 54</p></bio><email xlink:type="simple">nefrolog2013@mail.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-4526-8671</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Парастаева</surname><given-names>М. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Parastaeva</surname><given-names>M. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Парастаева Марина Магрезовна - старший научный сотрудник, канд. биол. наук, Научно-исследовательский институт нефрологии, лаборатория клинической физиологии почек,</p><p>197022, Санкт-Петербург, ул. Л. Толстого, д. 17, корп. 54</p></bio><bio xml:lang="en"><p>Parastaeva Marina M. - Senior Researcher,  PhD. Biol. sciences, Research Institute of Nephrology, Laboratory of Clinical Renal Physiology,</p><p>197022, St. Petersburg, L. Tolstogo str., 17, building 54</p></bio><email xlink:type="simple">marina_parastaeva@list.ru</email><xref ref-type="aff" rid="aff-3"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Румянцев</surname><given-names>А. Ш.</given-names></name><name name-style="western" xml:lang="en"><surname>Rumyantsev</surname><given-names>A. Sh.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Румянцев Александр Шаликович - проф., д-р мед. наук, кафедра факультетской терапии, 199106, Санкт-Петербург, 21-я линия В.О., д. 8а;</p><p>кафедра пропедевтики внутренних болезней, 197022, Санкт-Петербург, ул. Льва Толстого, д. 6–8</p></bio><bio xml:lang="en"><p>Rumyantsev Alexander Sh. - Prof., MD, PhD, DMedSci, department of faculty therapy,199106, St. Petersburg, 21st line V.O., 8a</p><p>Department of Propaedeutics of Internal Diseases,</p><p>197022, St. Petersburg, st. Leo Tolstoy, 6–8.</p></bio><email xlink:type="simple">rash.56@mail.ru</email><xref ref-type="aff" rid="aff-4"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-7532-2405</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Береснева</surname><given-names>О. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Beresneva</surname><given-names>O. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Береснева Ольга Николаевна - старший научный сотрудник, канд. биол. наук, Научно-исследовательский институт нефрологии, </p><p>197022, Санкт-Петербург, ул. Л. Толстого, д. 17, корп. 54</p></bio><bio xml:lang="en"><p>Beresneva Olga N. - Senior Researcher, PhD. Biol. sciences, Scientific Research Institute of Nephrology, Laboratory of Clinical Kidney Physiology,</p><p>197022, St. Petersburg, L. Tolstogo str., 17, building 54</p></bio><email xlink:type="simple">beresnevaolga@list.ru</email><xref ref-type="aff" rid="aff-3"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru">ФГБУН Институт физиологии им. И.П. Павлова РАН<country>Россия</country></aff><aff xml:lang="en">Pavlov Institute of Physiology, Russian Academy of Sciences<country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru">Первый Санкт-Петербургский государственный медицинский университет им. акад. И.П. Павлова<country>Россия</country></aff><aff xml:lang="en">Pavlov University<country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-3"><aff xml:lang="ru">Первый Санкт-Петербургский государственный медицинский университет им. акад. И.П. Павлова<country>Россия</country></aff><aff xml:lang="en">Institute of Nephrology, First Pavlov Saint-Petersburg State Medical University<country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-4"><aff xml:lang="ru">Санкт-Петербургский государственный университет;&#13;
Санкт-Петербургский государственный медицинский университет им. акад. И.П. Павлова<country>Россия</country></aff><aff xml:lang="en">Saint-Petersburg State University;&#13;
Pavlov St. Petersburg State Medical University<country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2024</year></pub-date><pub-date pub-type="epub"><day>07</day><month>03</month><year>2024</year></pub-date><volume>28</volume><issue>1</issue><fpage>105</fpage><lpage>115</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Иванова Г.Т., Хасун М.Х., Парастаева М.М., Румянцев А.Ш., Береснева О.Н., 2024</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="ru">Иванова Г.Т., Хасун М.Х., Парастаева М.М., Румянцев А.Ш., Береснева О.Н.</copyright-holder><copyright-holder xml:lang="en">Ivanova G.T., Khasun M.H., Parastaeva M.M., Rumyantsev A.S., Beresneva O.N.</copyright-holder><license 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://journal.nephrolog.ru/jour/article/view/2296">https://journal.nephrolog.ru/jour/article/view/2296</self-uri><abstract><sec><title>Введение</title><p>Введение. При хронической болезни почек (ХБП) часто наблюдаются кардиоваскулярные осложнения. Взаимоотношения между сердечно-сосудистой системой и почками сложны и многообразны, однако, вопрос о механизмах влияния избыточного потребления поваренной соли на функциональное состояние сосудов при дисфункции почек остается актуальным.</p></sec><sec><title>Цель</title><p>Цель: оценить влияние высокосолевого рациона на функциональное состояние сосудов микроциркуляторного русла (МЦР) кожи у крыс на ранней стадии дисфункции почек.</p></sec><sec><title>Материал и методы</title><p>Материал и методы. Исследование проведено на крысах Wistar. В первую SO-группу вошли животные, подвергнутые ложной операции (ЛО), получавшие стандартный рацион (0,34 % поваренной соли); во вторую HS-группу – животные, также подвергнутые ложной операции, но получавшие высокосолевую диету (4 % NaCl); в третью NE-группу – крысы, подвергнутые ¾ нефрэктомии (НЭ), получавшие стандартную диету; в четвертую HS+ NE-группу – крысы, подвергнутые ¾ НЭ, получавшие высокосолевой рацион (4 % NaCl). Артериальное давление (АД) измеряли на хвосте манжеточным методом («Систола», Россия), МЦР оценивали методом лазерной допплеровской флоуметрии («ЛДФ ЛАКК-ОП», Россия). Реактивность микрососудов кожи оценивали по изменению показателя МЦР до и после ионофореза ацетилхолина (АХ) и нитропруссида натрия (НП). На основании оценки спектральных характеристик флуктуаций показателя МЦР, полученных с помощью Вейвлет-анализа, рассчитывали величину эндотелиального, нейрогенного и миогенного тонуса микросоcудов.</p></sec><sec><title>Результаты</title><p>Результаты. Через 4 мес после ¾ НЭ у крыс отмечалось снижение экскреторной функции почек. У крыс на высокосолевой диете отмечалось увеличение уровня мочевины крови. Величина АД у крыс SO+HS-группы значимо не отличалась от контрольных животных SO-группы (131 ± 8 и 125 ± 4 мм рт. ст. соответственно, NS), НЭ приводила к значимому росту уровня АД (135 ± 5 мм рт. ст. у крыс NE-группы и 145 ± 7 мм рт. ст. – у NE+HS-группы). Средний показатель МЦР был больше у крыс, получавших высокосолевую диету (SO+HS- и NE+HS-группы), по сравнению с животными соответствующей группы, получавшими стандартный рацион. Сочетание НЭ и высокосолевой нагрузки оказывает ингибирующее влияние на амплитуду колебаний интенсивности перфузии во всех исследованных диапазонах: эндотелиальном, нейрогенном и миогенном, при этом расчетная величина тонуса микрососудов кожи в трех диапазонах оказалась наибольшей у крыс NE+HS-группы. Во всех экспериментальных группах реактивность на АХ была снижена по сравнению с SO-группой, а после ионофореза НП средний показатель перфузии значимо снижался только в группах животных, получавших высокосолевой рацион: SO+HS и NE+HS.</p></sec><sec><title>Заключение</title><p>Заключение. Высокосолевая диета у крыс с начальной стадией дисфункции почек способствует подъему уровня АД, снижению натрийуреза по сравнению с животными с НЭ, получавшими стандартный рацион. При избыточном потреблении поваренной соли у крыс после НЭ увеличивается интенсивность кожной МЦР при одновременном снижении вариативности показателя МЦР. Высокосолевая диета у крыс с НЭ модифицирует характеристики спектральных составляющих флуктуаций показателя МЦР, указывая на усиление тонических влияний на микрососуды кожи в эндотелиальном, нейрогенном и миогенном диапазонах. При гипернатриевой нагрузке у животных с ¾ НЭ наблюдается снижение реактивности кожных микрососудов на АХ и НП, которая опосредована как снижением продукции NO эндотелием, так и снижением чувствительности ГМК к NO.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Background</title><p>Background. Cardiovascular complications are common in chronic kidney disease (CKD). The relationship between the cardiovascular system and the kidneys is complex and diverse, but the question of the mechanisms of the influence of excess NaCl consumption on the functional state of blood vessels during renal dysfunction remains relevant.</p></sec><sec><title>The aim</title><p>The aim: to evaluate the effect of a high-salt diet on the functional state of microcirculatory vessels (MCR) of the skin in rats at an early stage of renal dysfunction.</p></sec><sec><title>Material and Methods</title><p>Material and Methods. The study was conducted on Wistar rats. The first SO group included animals subjected to sham surgery (SO) and receiving a standard diet (0.34% NaCl); in the second, HS group – animals that also underwent a sham operation, but received a high-salt diet (4% NaCl); in the third, NE group – rats subjected to ¾ nephrectomy (NE) and receiving a standard diet; the fourth, HS+ NE group included rats subjected to ¾ NE and fed a high-salt diet (4% NaCl). Blood pressure (BP) was measured in the tail using the cuff method (Sistola, Russia), MCR was assessed using laser Doppler flowmetry (LDF). The reactivity of skin microvessels was assessed by changes in the MCR index before and after iontophoresis of acetylcholine (ACh) and sodium nitroprusside (NP). Based on the assessment of the spectral characteristics of fluctuations in the MCR index obtained using Wavelet analysis, the value of endothelial, neurogenic and myogenic microvascular tone was calculated.</p></sec><sec><title>Results</title><p>Results. 4 months after ¾ NE, rats showed a decrease in the excretory function of the kidneys. In rats on a highsalt diet, an increase in blood urea levels was noted. The blood pressure in rats of the SO+HS group did not significantly differ from the control animals of the SO group (131 ± 8 and 125 ± 4 mmHg, respectively, NS), NE led to a significant increase in blood pressure (135 ± 5 mmHg in rats of the NE group, and 145 ± 7 mmHg – in the NE+HS group). The average MCR was higher in rats receiving a high-salt diet (SO+HS and NE+HS groups), compared with animals of the corresponding group receiving a standard diet. The combination of NE and high-salt load has an inhibitory effect on the amplitude of fluctuations in the intensity of perfusion in all studied ranges: endothelial, neurogenic and myogenic, while the calculated value of skin microvascular tone in three ranges was the highest in NE+HS group rats. In all experimental groups, the reactivity to AH was reduced compared with the SO group, and after NP iontophoresis, the average perfusion rate significantly decreased only in groups of animals receiving a high-salt diet: SO+HS and NE+HS.</p></sec><sec><title>Conclusion</title><p>Conclusion. A high-salt diet in rats with an initial stage of renal dysfunction contributes to an increase in blood pressure and a decrease in natriuresis compared with animals with NE who received a standard diet. With excessive consumption of table salt in rats after NE, the intensity of cutaneous MCR increases, while reducing the variability of the MCR index. A high-salt diet in rats with NE modifies the characteristics of the spectral components of fluctuations in the MCR index, indicating an increase in tonic effects on skin microvessels in the endothelial, neurogenic and myogenic ranges. With hypernatrial load, animals with ¾ NE have a decrease in the reactivity of cutaneous microvessels to AH and NP, which is mediated by both a decrease in endothelial NO production and a decrease in MMC sensitivity to NO.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>крысы</kwd><kwd>дисфункция почек</kwd><kwd>микроциркуляция</kwd><kwd>поваренная соль</kwd><kwd>артериальное давление</kwd><kwd>эксперимент</kwd></kwd-group><kwd-group xml:lang="en"><kwd>rats</kwd><kwd>kidney dysfunction</kwd><kwd>microcirculation</kwd><kwd>salt</kwd><kwd>blood pressure</kwd><kwd>experiment</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">Düsing P, Zietzer A, Goody PR, Hosen MR, Kurts C, Nickenig G, Jansen F. Vascular pathologies in chronic kidney disease: pathophysiological mechanisms and novel therapeutic approach- es. 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