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醛固酮是顽固性高血压中缺失的环节吗?:醛固酮与肾素比值作为醛固酮活性异常的标志物

Is aldosterone the missing link in refractory hypertension?: aldosterone-to-renin ratio as a marker of inappropriate aldosterone activity.

作者信息

Lim P O, Jung R T, MacDonald T M

机构信息

Department of Cardiology, Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, Wales, UK.

出版信息

J Hum Hypertens. 2002 Mar;16(3):153-8. doi: 10.1038/sj.jhh.1001320.

DOI:10.1038/sj.jhh.1001320
PMID:11896503
Abstract

Use of the random aldosterone-to-renin ratio (ARR) as a reliable marker of inappropriate aldosterone activity has led to primary aldosteronism (PA) being increasingly diagnosed in hypertensive patients. At least 10% of hypertensives have been found to have PA, the majority of whom presumably have bilateral adrenal hyperplasia or idiopathic hyperaldosteronism as an aetiology for PA. Whilst these patients clearly have excess aldosterone activity, they have in common many features that are found in hypertensive patients in general, amongst which include heightened angiotensin II adrenal sensitivity. Whether these individuals belong within the spectrum of 'essential hypertension' is being debated, but is probably irrelevant clinically since they appear to respond favourably to spironolactone treatment. In addition, there is recent evidence suggesting that these patients overexpress a key enzyme involved in aldosterone production, the aldosterone synthase, the activity of which appears to relate to its genotypic variation.

摘要

使用随机醛固酮与肾素比值(ARR)作为不适当醛固酮活性的可靠标志物,已导致原发性醛固酮增多症(PA)在高血压患者中越来越多地被诊断出来。至少10%的高血压患者被发现患有PA,其中大多数可能患有双侧肾上腺增生或特发性醛固酮增多症作为PA的病因。虽然这些患者显然存在醛固酮活性过高的情况,但他们具有许多一般高血压患者共有的特征,其中包括血管紧张素II肾上腺敏感性增强。这些个体是否属于“原发性高血压”范畴仍存在争议,但在临床上可能无关紧要,因为他们似乎对螺内酯治疗反应良好。此外,最近有证据表明,这些患者过度表达一种参与醛固酮生成的关键酶——醛固酮合酶,其活性似乎与其基因型变异有关。

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NP-59 SPECT/CT imaging in stage 1 hypertensive and atypical primary aldosteronism: a 5-year retrospective analysis of clinicolaboratory and imaging features.1期高血压和非典型原发性醛固酮增多症的NP-59 SPECT/CT成像:临床实验室和影像特征的5年回顾性分析
ScientificWorldJournal. 2013 Oct 21;2013:317934. doi: 10.1155/2013/317934. eCollection 2013.
2
Kininogen gene (KNG) variation has a consistent effect on aldosterone response to antihypertensive drug therapy: the GERA study.激肽原基因(KNG)变异对降压药物治疗后醛固酮反应的影响具有一致性:GERA 研究。
Physiol Genomics. 2009 Sep 9;39(1):56-60. doi: 10.1152/physiolgenomics.00061.2009. Epub 2009 Jul 7.
3
TASK channel deletion in mice causes primary hyperaldosteronism.
小鼠体内TASK通道缺失会导致原发性醛固酮增多症。
Proc Natl Acad Sci U S A. 2008 Feb 12;105(6):2203-8. doi: 10.1073/pnas.0712000105. Epub 2008 Feb 4.
4
Adding low-dose spironolactone to multidrug regimens for resistant hypertension.
Curr Hypertens Rep. 2004 Jun;6(3):211-2.