Zschiedrich H, Fleckenstein P, Geiger R, Fink E, Sinterhauf K, Philipp T, Distler A, Wolff H P
Clin Exp Hypertens (1978). 1980;2(3-4):693-708. doi: 10.3109/10641968009037137.
Basal 24 hour urinary kallikrein excretion of 20 patients with uncomplicated essential hypertension did not differ significantly from that of 18 normotensive age-matched control subjects. 4 of the 20 hypertensive patients, however, had low kallikrein excretion. Furosemide (40 mg i.v.) caused an increase of urinary kallikrein excretion in the normotensive subjects and in most of the patients with essential hypertension. The stimulating effect of furosemide was less pronounced or even absent in 7 hypertensives. No circadian rhythm of urinary kallikrein excretion was observed. There were weak correlations between 24 hour kallikrein excretion and urinary volume (r=0.59; p < 0.05), and potassium excretion (r=0.51; p < 0.05) in the normotensives. In the hypertensives correlations were found between 24 hour kallikrein excretion and potassium excretion (r=0.51; p < 0.05), aldosterone excretion (r=0.57; p < 0.01), and creatinine clearance (r=0.59; p < 0.01). Our findings do not support the concept that the renal kallikrein-kinin system might play a primary role in the pathogenesis of essential hypertension.
20例无并发症的原发性高血压患者的基础24小时尿激肽释放酶排泄量与18例年龄匹配的血压正常对照者相比，无显著差异。然而，20例高血压患者中有4例激肽释放酶排泄量较低。速尿（静脉注射40毫克）可使血压正常者和大多数原发性高血压患者的尿激肽释放酶排泄量增加。速尿的刺激作用在7例高血压患者中不明显甚至没有。未观察到尿激肽释放酶排泄的昼夜节律。血压正常者中，24小时激肽释放酶排泄量与尿量（r = 0.59；p < 0.05）和钾排泄量（r = 0.51；p < 0.05）之间存在弱相关性。在高血压患者中，发现24小时激肽释放酶排泄量与钾排泄量（r = 0.51；p < 0.05）、醛固酮排泄量（r = 0.57；p < 0.01）和肌酐清除率（r = 0.59；p < 0.01）之间存在相关性。我们的研究结果不支持肾激肽释放酶-激肽系统在原发性高血压发病机制中可能起主要作用的观点。
