正常血压受试者和原发性高血压患者的尿激肽释放酶
Urinary kallikrein in normotensive subjects and in patients with essential hypertension.
作者信息
Zschiedrich H, Fleckenstein P, Geiger R, Fink E, Sinterhauf K, Philipp T, Distler A, Wolff H P
出版信息
Clin Sci (Lond). 1979 Dec;57 Suppl 5:247s-250s. doi: 10.1042/cs057247s.
PMID:396074
Abstract
- Excretion of urinary kallikrein was normal in 13 out of 15 patients with uncomplicated essential hypertension. 2. Frusemide increased urinary kallikrein excretion in normotensive subjects and in patients with essential hypertension. The stimulating effect of frusemide on urinary kallikrein was significantly diminished in patients with essential hypertension. 3. No correlations of urinary kallikrein with sodium, potassium, and aldosterone excretion were found. 4. The results do not support the idea that urinary kallikrein plays a primary role in the pathogenesis of essential hypertension.
摘要
- 15例无并发症的原发性高血压患者中，13例尿激肽释放酶排泄正常。2. 速尿可增加血压正常者及原发性高血压患者的尿激肽释放酶排泄。速尿对原发性高血压患者尿激肽释放酶的刺激作用明显减弱。3. 未发现尿激肽释放酶与钠、钾及醛固酮排泄之间存在相关性。4. 这些结果不支持尿激肽释放酶在原发性高血压发病机制中起主要作用这一观点。
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引用本文的文献
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[Renal kallikrein-kinin system and control of blood pressure (author's transl)].肾激肽释放酶-激肽系统与血压调控（作者译）
Klin Wochenschr. 1979 Oct 1;57(19):1037-45. doi: 10.1007/BF01479989.
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