nefrНефрологияNephrology (Saint-Petersburg)1561-62742541-9439Pavlov First Saint-Petersburg State Medical University10.24884/1561-6274-2019-23-5-96-101nefr-1748Research ArticleОРИГИНАЛЬНЫЕ СТАТЬИ. ЭКСПЕРИМЕНТАЛЬНЫЕ ИССЛЕДОВАНИЯORIGINAL ARTICLES. EXPERIMENTAL INVESTIGATIONNO-зависимый механизм вазодилатации в пиальных артериях нефрэктомированных крысNO-dependent mechanism of vasodilation in pial arteries of nefrectomizedratshttps://orcid.org/0000-0002-7483-1080СоколоваИ. Б.SokolovaI. B.

Соколова Ирина Борисовна – старший научный сотрудник, Лаборатория физиологии сердечно-сосудистой и лимфатической систем.

199034, Санкт-Петербург, наб. Макарова, д. 6.

Тел.: 8(813) 70-71-553.

Sokolova Irina Borisovna - senior researcher, Laboratory of physiology of cardiovascular and lymphatic systems.

199934, Makarova Emb., 6., Saint-Petersburg.

Ph. 8(813) 70- 71-553.

SokolovaIB@infran.ruhttps://orcid.org/0000-0003-0188-5173ИвановаГ. Т.IvanovaG. T.

Иванова Галина Тажимовна - старший научный сотрудник, Лаборатория физиологии сердечно-сосудистой и лимфатической систем.

199034, Санкт-Петербург, наб. Макарова, д. 6.

Тел.: 8 (812) 328-07-01.

Ivanova Galina Tazhimovna - senior researcher, Laboratory of physiology of cardiovascular and lymphatic systems.

199034, Makarova Emb., 6, Saint-Petersburg.

Ph. 8 (812) 328-07-01.

tazhim@list.ruhttps://orcid.org/0000-0003-3088-4647ЛобовГ. И.LobovG. I.

Лобов Геннадий Иванович - заведующий лабораторией, Лаборатория физиологии сердечно-сосудистой и лимфатической систем.

199034, Санкт-Петербург, наб. Макарова, д. 6.

Тел.: +7 921 7430608.

Lobov Gennadii Ivanovich - head of laboratory, Laboratory of physiology of cardiovascular and lymphatic systems.

199934, Makarova Emb., 6., Saint-Petersburg.

Ph. +7 921 7430608.

LobovGI@infran.ruИнститут физиологии им. И.П. Павлова РАНРоссияInstitute of physiology I. P. Pavlov of the Russian Academy of SciencesRussian Federation20190808201923596101Copyright © Соколова И.Б., Иванова Г.Т., Лобов Г.И., 20192019Соколова И.Б., Иванова Г.Т., Лобов Г.И.Sokolova I.B., Ivanova G.T., Lobov G.I.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://journal.nephrolog.ru/jour/article/view/1748ЦЕЛЬ

ЦЕЛЬ: изучить изменения NO-опосредованного механизма дилатации в пиальных артериях головного мозга нефрэктомированных крыс.

МАТЕРИАЛ И МЕТОДЫ

МАТЕРИАЛ И МЕТОДЫ: исследование проведено на крысах линии Wistar–Kyoto (WKY). В 4-месячном возрасте проводили двухэтапную нефрэктомию. Через 3 мес методом прижизненной микроскопии исследовали реакции артерий пиальной оболочки головного мозга на агонисты и антагонисты (измеряли диаметр артерий на фоне действия ацетилхолина, нитропруссида натрия и метиленового голубого). Помимо этого, измеряли перфузию ткани мозга с целью последующих расчетов величин компонентов сосудистого тонуса.

РЕЗУЛЬТАТЫ

РЕЗУЛЬТАТЫ: показано, что аппликация ацетилхолина на пиальную оболочку приводила к изменению диаметра артерий. У нефрэктомированных крыс при действии АХ было зарегистрировано значительно большее количество артерий в состоянии констрикции по сравнению с контрольной группой. Действие нитропруссида натрия в контрольной группе сопровождалось дилатацией 100 % пиальных артерий, в группе нефрэктомированных крыс дилатация была выявлена в 83,2±4,7 % артерий. При применении метиленового голубого в группе нефрэктомированных крыс было выявлено меньшее количество артерий в состоянии констрикции по сравнению с контрольной группой.

ЗАКЛЮЧЕНИЕ

ЗАКЛЮЧЕНИЕ: у нефрэктомированных крыс выявлены выраженные нарушения NO-опосредованного механизма дилатации пиальных артерий головного мозга, приводящие к повышению эндотелиального компонента сосудистого тонуса. Эндотелий пиальных артерий нефрэктомированных крыс продуцирует меньшее количество NO как спонтанно, так и при стимуляции ацетилхолином. У нефрэктомированных крыс выявлены нарушения в сигнальном каскаде NO→sGC→cGMP в ГМК пиальных артерий, что подтверждается их меньшей способностью к дилатации на применение экзогенного NO.

THE AIM

THE AIM: to study changes in the NO-mediated dilatation mechanism in the pial arteries of the brain of nephrectomized rats.

MATERIALS AND METHODS

MATERIALS AND METHODS: The study was conducted on Wistar-Kyoto rats. At 4 months of age, a two-stage nephrectomy was performed. After 3 months, the reaction of the arteries of the pial membrane of the brain to agonists and antagonists was investigated by in vivo microscopy (the diameter of the arteries was measured against the action of acetylcholine, sodium nitroprusside and methylene blue). Besides, the perfusion of the brain tissue was measured for subsequent calculations of the values of the components of the vascular tone.

RESULTS

RESULTS: It was shown that the application of acetylcholine to the pial membrane led to a change in the diameter of the arteries. In nephrectomized rats under the action of acetylcholine, a significantly larger number of arteries in the constriction state was registered compared to the control group. The effect of sodium nitroprusside in the control group was accompanied by a dilatation of 100 % of the pial arteries; in the nephrectomized rat group, dilatation was detected in 83.2 ± 4.7 % of the arteries. When methylene blue was used in a group of nephrectomized rats, a smaller number of arteries in the constriction state was detected as compared to the control group.

CONCLUSION

CONCLUSION: In nephrectomized rats, pronounced disorders of the NO-mediated mechanism of the pial arteries of the brain were found, leading to an increase in the endothelial component of the vascular tone. The endothelium of the pial arteries of nephrectomized rats produces less NO both spontaneously and when stimulated with acetylcholine. In nephrectomized rats, abnormalities in the signal cascade of NO →sGC → cGMP in the smooth muscle cells of the pial arteries were revealed, which is confirmed by their lesser ability to dilate to the use of exogenous NO.

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The authors declare that there are no conflicts of interest present.