Inappropriate activity of local renin-angiotensin-aldosterone system during high salt intake: impact on the cardio-renal axis

ABSTRACT Although there is a general agreement on the recommendation for reduced salt intake as a public health issue, the mechanism by which high salt intake triggers pathological effects on the cardio-renal axis is not completely understood. Emerging evidence indicates that the renin-angiotensin-aldosterone system (RAAS) is the main target of high Na+ intake. An inappropriate activation of tissue RAAS may lead to hypertension and organ damage. We reviewed the impact of high salt intake on the RAAS on the cardio-renal axis highlighting the molecular pathways that leads to injury effects. We also provide an assessment of recent observational studies related to the consequences of non-osmotically active Na+ accumulation, breaking the paradigm that high salt intake necessarily increases plasma Na+ concentration promoting water retention摘要：尽管将减少盐摄入作为公共卫生议题已达成广泛共识，但高盐摄入触发心肾轴（cardio-renal axis）产生病理效应的具体机制仍未完全阐明。越来越多的证据表明，肾素-血管紧张素-醛固酮系统（renin-angiotensin-aldosterone system, RAAS）是高钠离子（Na+）摄入的主要作用靶点。组织RAAS的异常激活可引发高血压与器官损伤。本综述探讨了高盐摄入对心肾轴内RAAS的影响，重点阐明了介导其损伤效应的分子通路。此外，本综述还评估了近期围绕非渗透性活性钠离子（non-osmotically active Na+）蓄积相关后果开展的观察性研究，打破了"高盐摄入必然会升高血浆钠离子浓度并促进水潴留"的固有认知。