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高血压与果糖和高盐相关:肾脏和交感神经机制。

Hypertension Associated with Fructose and High Salt: Renal and Sympathetic Mechanisms.

机构信息

Department of Physiology, Wayne State University, 4160 John R Street #908, Detroit, MI 48201, USA.

Department of Internal Medicine, Wayne State University, 4160 John R Street #908, Detroit, MI 48201, USA.

出版信息

Nutrients. 2019 Mar 7;11(3):569. doi: 10.3390/nu11030569.

DOI:10.3390/nu11030569
PMID:30866441
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6472002/
Abstract

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.

摘要

高血压是心血管疾病和慢性肾病的主要病因。尽管我们在理解高血压的病因方面取得了许多重要的进展,但由于多种因素,包括环境、遗传和饮食,其机制仍然很复杂。本篇综述重点关注饮食因素的贡献,提供了证据表明,高果糖和盐的摄入与全球范围内高血压发病率的上升有关。高果糖负荷会增强肾脏对盐的重吸收,导致血压升高。在这种环境下,几种转运蛋白,如 NHE3 和 PAT1 被调节,在盐敏感性中发挥着关键作用。高果糖摄入还会调节肾素-血管紧张素-醛固酮系统。最近的研究重点转向了交感神经系统的贡献,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,在果糖诱导的盐敏感性高血压中,肾交感神经被激活,肾神经消融后血压降低。这篇综述进一步证明了肾脏对钠的处理、肾素-血管紧张素-醛固酮系统以及肾交感神经的激活之间的相互作用,是果糖和盐诱导高血压的重要机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8247/6472002/35540687452b/nutrients-11-00569-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8247/6472002/35540687452b/nutrients-11-00569-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8247/6472002/35540687452b/nutrients-11-00569-g001.jpg

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