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肾脏对交感神经系统的调节。

Regulation of the sympathetic nervous system by the kidney.

机构信息

aNeurovascular Hypertension and Kidney Disease Laboratory, Baker IDI Heart and Diabetes Institute bSchool of Public Health and Preventive Medicine, Monash University cHeart Centre Alfred Hospital dFaculty of Medicine, Nursing and Health Sciences and Department of Physiology, Monash University, Melbourne, Australia.

出版信息

Curr Opin Nephrol Hypertens. 2014 Jan;23(1):61-8. doi: 10.1097/01.mnh.0000437610.65287.db.

Abstract

PURPOSE OF REVIEW

The relationship between excessive sympathetic drive to the kidneys and hypertension is now well established. This has led to the development of therapeutic approaches, such as catheter-based bilateral renal denervation, for the treatment of resistant hypertension. The purpose of this article is to review the sympathetic regulation of kidney function, with specific focus given to clinical insights gained from human studies involving renal denervation and animal studies that have identified possible causal factors associated with disease.

RECENT FINDINGS

Continuous chronic determinations of renal sympathetic nerve activity (RSNA) in animal models have recently identified a role of angiotensin II and obesity in the initiation of neurally related hypertension. Other potential mediating factors influencing RSNA include adipose tissue derived factors, neurohumoral pathways and baroreceptor-mediated mechanisms. Hypertension development is likely to reflect a combination of these factors. Interventions that directly interrupt renal sympathetic signaling show promising results in the treatment of resistant hypertension.

SUMMARY

The mechanisms underlying the development of neurogenic hypertension are beginning to be elucidated, thanks to technological advancements that enable the direct measurement of RSNA. Determining factors associated with hypertension development will help to identify strategies to mitigate disease as well as provide scientific support for novel nonpharmacologic therapies.

摘要

目的综述

目前,肾脏过度交感神经驱动与高血压之间的关系已得到充分证实。这促使人们开发了治疗方法,如基于导管的双侧肾脏去神经支配术,以治疗难治性高血压。本文旨在综述肾脏交感神经调节的功能,特别关注涉及肾脏去神经支配的人体研究和确定与疾病相关的可能因果因素的动物研究中获得的临床见解。

最新发现

最近,在动物模型中对肾脏交感神经活动(RSNA)进行连续慢性测定,确定了血管紧张素 II 和肥胖在神经相关性高血压发生中的作用。影响 RSNA 的其他潜在介导因素包括脂肪组织衍生因子、神经体液途径和压力感受器介导的机制。高血压的发展可能反映了这些因素的综合作用。直接阻断肾脏交感神经信号的干预措施在治疗难治性高血压方面显示出良好的效果。

总结

由于能够直接测量 RSNA 的技术进步,神经原性高血压发展的机制开始得到阐明。确定与高血压发展相关的因素将有助于确定减轻疾病的策略,并为新型非药物治疗提供科学依据。

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