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肾脏、盐与高血压关系的最新进展。

An update on the relationship between the kidney, salt and hypertension.

作者信息

Mayer Gert

机构信息

Division of Nephrology and Hypertensiology, Department of Internal Medicine IV, Innsbruck, Austria.

出版信息

Wien Med Wochenschr. 2008;158(13-14):365-9. doi: 10.1007/s10354-008-0559-2.

DOI:10.1007/s10354-008-0559-2
PMID:18677586
Abstract

The relationship between salt intake and blood pressure has been noteworthy for a long time. Nevertheless, the complex hemodynamic alterations associated with the salt-induced blood pressure changes have become clear only quite recently. Despite this knowledge, the concept of Guyton, which postulates that any increase in blood pressure should lead to a pressure natriuresis normalising blood pressure over the long term is still valid. As a conclusion, we have to remember that an elevation of arterial pressure can only be maintained if renal function as indicated by pressure natriuresis is impaired.

摘要

长期以来,盐摄入量与血压之间的关系一直备受关注。然而,与盐诱导的血压变化相关的复杂血流动力学改变直到最近才变得清晰。尽管有了这些认识,但盖顿的概念仍然有效,该概念假定任何血压升高最终都应导致压力性利钠作用使血压恢复正常。总之,我们必须记住,只有当压力性利钠作用所指示的肾功能受损时,动脉血压升高才能持续存在。

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本文引用的文献

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Pathophysiological mechanisms of salt-dependent hypertension.盐依赖性高血压的病理生理机制。
Am J Kidney Dis. 2007 Oct;50(4):655-72. doi: 10.1053/j.ajkd.2007.05.025.
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Evolution and hypertension.
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Device-guided slow-breathing effects on end-tidal CO(2) and heart-rate variability.仪器引导的缓慢呼吸对潮气末二氧化碳和心率变异性的影响。
Psychol Health Med. 2009 Dec;14(6):667-79. doi: 10.1080/13548500903322791.
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Mechanisms of disease: oxidative stress and inflammation in the pathogenesis of hypertension.疾病机制:高血压发病机制中的氧化应激与炎症
Nat Clin Pract Nephrol. 2006 Oct;2(10):582-93. doi: 10.1038/ncpneph0283.
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Salt intake and depletion increase circulating levels of endogenous ouabain in normal men.盐摄入与缺失会增加正常男性体内内源性哇巴因的循环水平。
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Rostafuroxin: an ouabain antagonist that corrects renal and vascular Na+-K+- ATPase alterations in ouabain and adducin-dependent hypertension.罗斯他福罗辛:一种哇巴因拮抗剂,可纠正哇巴因和内收蛋白依赖性高血压中肾脏和血管的钠钾ATP酶改变。
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