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高血压患者尿激肽释放酶异常与醛固酮或血浆肾素活性无关。

Abnormal urinary kallikrein in hypertension is not related to aldosterone or plasma renin activity.

作者信息

Lawton W J, Fitz A E

出版信息

Hypertension. 1980 Nov-Dec;2(6):787-93. doi: 10.1161/01.hyp.2.6.787.

DOI:10.1161/01.hyp.2.6.787
PMID:7007236
Abstract

The relationships between urinary kallikrein (Ukal), and plasma renin activity (PRA), urinary aldosterone (Ualdo), Na+ balance, SK+, and renal function were studied in essential hypertensives (EHT) and normals. Ukal was measured by a radiochemical esterolytic assay. We studied 18 white patients with EHT (15 men, 3 women) ages 31.6 to +/- 2.1 (SEM) yrs, BP 138 +/- 2/95 +/- 2 mm Hg. and 12 white normals (NLS) (7 men, 5 women) ages 30.2 +/- 2.3 yrs, BP 112 +/- 4/71 +/- 2 mm Hg. All received a 5-day diet of 400 mEq Na+, 80 mEq K+/day, and 5 days of 10 mEq Na+, 80 mEq K+/day. All achieved Na+ balance by Day 5. On Day 5 of the low Na+ diet, 24 hr. Ukal in EHT was 15.8 +/- 2.4 (esterase units/24 hr) vs NLS, 17.0 +/- 2.8 PRA was the same in EHT and NLS, but Ualdo was higher in NLS. (Day 5, low Na+, EHT, Ualdo = 29.4 +/0 3.3 microgram/24h. vs NLS 41.8 +/- 4.7, p less than 0.02). Analysis of individuals showed that all NLS increased Ukal after salt restriction, while 3 EHT decreased Ukal after salt restriction. This abnormal response in EHT was not related to abnormalities in Ualdo, PRA, Na+ balance, SK+, or creatinine clearance. In 3 EHT with low-renin EHT, the Ukal response was normal. In two of four patients with primary aldosteronism, Ukal was normal despite increased Ualdo. The Ukal response to salt restriction is abnormal in some EHT, unrelated to Ualdo or PRA, suggesting either a primary defect in Ukal and/or the presence of other factors modulating Ukal in EHT.

摘要

在原发性高血压患者(EHT)和正常人中研究了尿激肽释放酶(Ukal)与血浆肾素活性(PRA)、尿醛固酮(Ualdo)、钠平衡、血清钾(SK +)及肾功能之间的关系。采用放射化学酯水解测定法测量Ukal。我们研究了18例年龄为31.6±2.1(SEM)岁的白人EHT患者(15例男性,3例女性),血压为138±2/95±2 mmHg,以及12例年龄为30.2±2.3岁的白人正常人(NLS)(7例男性,5例女性),血压为112±4/71±2 mmHg。所有人均接受了为期5天、每天摄入400 mEq钠、80 mEq钾的饮食,以及为期5天、每天摄入10 mEq钠、80 mEq钾的饮食。到第5天时所有人均实现了钠平衡。在低钠饮食的第5天,EHT患者的24小时Ukal为15.8±2.4(酯酶单位/24小时),而NLS为17.0±2.8。EHT和NLS的PRA相同,但NLS的Ualdo更高。(低钠饮食第5天,EHT患者的Ualdo = 29.4±3.3微克/24小时,而NLS为41.8±4.7,p<0.02)。个体分析显示,所有NLS在限盐后Ukal升高,而3例EHT患者在限盐后Ukal降低。EHT患者的这种异常反应与Ualdo、PRA、钠平衡、血清钾或肌酐清除率的异常无关。在3例低肾素型EHT患者中,Ukal反应正常。在4例原发性醛固酮增多症患者中的2例中,尽管Ualdo升高,但Ukal正常。一些EHT患者对限盐的Ukal反应异常,与Ualdo或PRA无关,提示EHT患者中Ukal存在原发性缺陷和/或存在其他调节Ukal的因素。

相似文献

1
Abnormal urinary kallikrein in hypertension is not related to aldosterone or plasma renin activity.高血压患者尿激肽释放酶异常与醛固酮或血浆肾素活性无关。
Hypertension. 1980 Nov-Dec;2(6):787-93. doi: 10.1161/01.hyp.2.6.787.
2
Urinary kallikrein in normal renin essential hypertension.正常肾素型原发性高血压中的尿激肽释放酶
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Direct and indirect measurement of urinary kallikrein excretion in patients with essential hypertension and normotensives: relation to age and plasma renin and aldosterone levels.原发性高血压患者和血压正常者尿激肽释放酶排泄的直接和间接测量:与年龄、血浆肾素和醛固酮水平的关系。
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Urinary kallikrein excretion in essential and mineralocorticoid hypertension.原发性高血压和盐皮质激素性高血压患者的尿激肽释放酶排泄情况。
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Urinary excretion of kallikrein before and after operation for aldosterone-producing adenoma.醛固酮分泌性腺瘤手术前后的激肽释放酶尿排泄量。
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Urinary kallikrein and plasma renin activity as determinants of renal blood flow. The influence of race and dietary sodium intake.尿激肽释放酶和血浆肾素活性作为肾血流量的决定因素。种族和饮食钠摄入量的影响。
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Non-modulating hypertension: evidence for the involvement of kallikrein/kinin activity associated with overactivity of the renin-angiotensin system. Successful blood pressure control during long-term Na+ restriction.非调节性高血压:与肾素-血管紧张素系统过度活跃相关的激肽释放酶/激肽活性参与的证据。长期限钠期间成功控制血压。
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Potassium supplementation lowers blood pressure and increases urinary kallikrein in essential hypertensives.补充钾可降低原发性高血压患者的血压并增加尿激肽释放酶。
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Renal kallikrein-kinin system and prostaglandin in hypertension: their relation to renin-angiotensin-aldosterone system.高血压中的肾激肽释放酶-激肽系统和前列腺素:它们与肾素-血管紧张素-醛固酮系统的关系。
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Urinary kallikrein excretion in patients with primary aldosteronism: differentiation of adrenal adenoma from idiopathic adrenal hyperplasia.原发性醛固酮增多症患者的尿激肽释放酶排泄:肾上腺腺瘤与特发性肾上腺增生的鉴别
Urol Int. 1984;39(1):40-5. doi: 10.1159/000280942.

引用本文的文献

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