nefrНефрологияNephrology (Saint-Petersburg)1561-62742541-9439Pavlov First Saint-Petersburg State Medical University10.24884/1561-6274-2008-12-2-39-46nefr-1049Research ArticleОБЗОРЫ И ЛЕКЦИИREVIEWS AND LECTURESПОЧЕЧНЫЕ МЕХАНИЗМЫ НЕФРОГЕННОЙ АРТЕРИАЛЬНОЙ ГИПЕРТОНИИRENAL MECHANISMS OF NEPHROGENIC ARTERIAL HYPERTENSIONКузьминО. Б.KuzminO. B.

Кафедра фармакологии

460040, г. Оренбург, пр. Гагарина 40/2.

ПугаеваМ. О.PugaevaM. O.

Кафедра фармакологии

460040, г. Оренбург, пр. Гагарина 40/2.

БучневаН. В.BuchnevaN. V.

Кафедра фармакологии

460040, г. Оренбург, пр. Гагарина 40/2.

Оренбургская государственная медицинская академияRussian Federation2008100220081223946Copyright © Кузьмин О.Б., Пугаева М.О., Бучнева Н.В., 20082008Кузьмин О.Б., Пугаева М.О., Бучнева Н.В.Kuzmin O.B., Pugaeva M.O., Buchneva N.V.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/1049

Артериальная гипертензия (АГ) у больных с хронической почечной патологией является следствием повреждения и нарушения функции почек, участвующих в поддержании вводно-солевого и циркуляторного гомеостаза. Прогрессирующее повреждение почечной ткани, помимо активации циркулирующей ренин-ангиотензин-альдостероновой системы (РААС), характерной для гиперрениновой формы нефрогенной АГ, вызывает рефлекторную стимуляцию центральных структур симпатической нервной системы (СНС), которая ведет к нарастающему увеличению симпатических влияний на сердечно-сосудистую систему и почки. Характерной чертой нейрогуморального статуса больных с нормо- и, особенно, гипорениновой форм нефрогенной АГ является повышение активности эндотелиновой (ЭТ) системы сосудов. Формирование в почках дисбаланса нейрогуморальных систем сопровождается избыточной реабсорбцией натрия, которая не только подавляет механизм прессорного натрийуреза, способствуя стабилизации АД на более высоком уровне, но и вызывает задержку его в организме, обеспечивая развитие объемзависмой и солечувствительной АГ.

Arterial hypertension (AH) in patients with chronic renal pathology is a result of a damage and impaired function of the kidneys involved in the maintenance of the water-salt and circulatory homeostasis. The progressing damage of the renal tissue, in addition to activation of the circulating renin-angiotensin- aldosterone system (RAAS) characteristic of the hyper-renin form of nephrogenic AH, brings on reflectory stimulation of the central structures sympathetic system, which lead to growing sympathetic influence on the cardiovascular system and kidneys. A characteristic feature of the neuro-humoral status of patients with normo- , and especially with hyporenin forms of nephrogenic AH is an elevated activity of endothelin system of the vessels. Formed in the kidneys disbalance of neurohumoral systems is accompanied by excessive reabsorption of sodium, which not only suppresses the mechanism of pressor natriuresis contributing to stabilization of AH at a higher level, but causes its delay in organism, providing for the development of volume-dependent and salt-sensitive AH.

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