Hypertension Associated with Fructose and High Salt: Renal and Sympathetic Mechanisms
Hypertension Associated with Fructose and High Salt: Renal and Sympathetic Mechanisms
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DOI：
10.3390/nu11030569
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发表时间：
2019-03-07
期刊：
影响因子：
5.9
通讯作者：
Rossi, Noreen F.
中科院分区：
文献类型：
--
作者：
Komnenov, Dragana;Levanovich, Peter E.;Rossi, Noreen F.
高血压是心血管和慢性肾脏疾病的主要原因。尽管我们对高血压病因的理解取得了多项重要进展，但由于环境、遗传和饮食等多种因素，其机制仍然很复杂。这篇综述的重点是饮食方面的贡献，为果糖和盐摄入的增加与世界范围内高血压发病率的增加有关提供证据。高果糖负荷增强了肾脏对盐的重吸收，导致血压升高。几种转运蛋白，如NHE3和PAT1在这种环境中被调节，并在盐敏感性中发挥关键作用。高果糖摄入也调节肾素-血管紧张素-醛固酮系统。最近的注意力已经转移到交感神经系统的作用上，因为临床试验表明肾交感神经消融后血压显著降低。新的临床前数据表明，果糖诱导的盐敏感性高血压可激活肾交感神经，肾神经消融后可降低血压。这篇综述进一步证明了肾脏处理钠、肾素-血管紧张素-醛固酮系统和肾交感神经激活之间的相互作用是果糖和盐诱导高血压的重要机制。
Hypertension is a leading cause of cardiovascular and chronic renal disease. Despite multiple important strides that have been made in our understanding of the etiology of hypertension, the mechanisms remain complex due to multiple factors, including the environment, heredity and diet. This review focuses on dietary contributions, providing evidence for the involvement of elevated fructose and salt consumption that parallels the increased incidence of hypertension worldwide. High fructose loads potentiate salt reabsorption by the kidney, leading to elevation in blood pressure. Several transporters, such as NHE3 and PAT1 are modulated in this milieu and play a crucial role in salt-sensitivity. High fructose ingestion also modulates the renin-angiotensin-aldosterone system. Recent attention has been shifted towards the contribution of the sympathetic nervous system, as clinical trials demonstrated significant reductions in blood pressure following renal sympathetic nerve ablation. New preclinical data demonstrates the activation of the renal sympathetic nerves in fructose-induced salt-sensitive hypertension, and reductions of blood pressure after renal nerve ablation. This review further demonstrates the interplay between sodium handling by the kidney, the renin-angiotensin-aldosterone system, and activation of the renal sympathetic nerves as important mechanisms in fructose and salt-induced hypertension.