m+Medelevator.RU
← Поиск публикаций
Scientific reports · 2017

Involvement of Epithelial Na+ Channel in the Elevated Myogenic Response in Posterior Cerebral Arteries from Spontaneously Hypertensive Rats.

СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…

История · было → стало

Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.

Choi Soo-Kyoung, Yeon Soo-In, Kwon Youngin, Byeon Seonhee, Lee Young-Ho

Аннотация

Hypertension is characterized by increased peripheral vascular resistance which is related with elevated myogenic response. Recent findings have indicated that epithelial sodium channel (ENaC) is involved in mechanotransduction of the myogenic response. The purpose of this study was to investigate the involvement of ENaC in the elevated myogenic response of posterior cerebral arteries (PCAs) from spontaneously hypertensive rats (SHRs). Sixteen to eighteen weeks old male wistar kyoto rats (WKYs) and SHRs were used in this study. We found that wall to lumen (W/L) ratio was increased in the PCAs from SHRs compared with WKYs at the resting state. Interestingly, amiloride significantly inhibited myogenic response in the PCAs from SHRs and WKYs, however, the magnitude of the blockade was greater in SHRs. The transfection of γENaC-siRNA significantly reduced the expression of γENaC protein and inhibited myogenic response in the PCAs from SHRs. Furthermore, these data were supported by the findings that serum/glucocorticoid-induced kinase (Sgk1) and neural precursor cell-expressed developmentally downregulated gene 4-2 (Nedd4-2) were increased in SHRs compared with WKYs. Our results suggest that γENaC may play an important role in the elevated myogenic response in PCAs from SHRs.

Предметные рубрики MeSH

ИП Урсолов Владлен Сергеевич

ИНН 500118482352 · ОГРНИП 314500117700049

Реквизиты и контакты