Overlack A, Stumpe K O, Ressel C, Kolloch R, Zywzok W, Krück F
Klin Wochenschr. 1980 Jan 2;58(1):37-42. doi: 10.1007/BF01477142.
Urinary kallikrein excretion was significantly lower in patients with essential hypertension (0.48 +/- 0.05 EU/24 h) than in normotensive controls (1.26 +/- 0.14 EU/24 h). Oral administration of hog pancreatic kallikrein normalized decreased urinary kallikrein and reduced arterial pressure. The treatment-induced rise in urinary kallikrein was due to an enhanced release of endogenous enzyme, as was determined by radioimmunoassay. It is proposed that in the hypertensive patients the low urinary kallikrein excretion reflects a defect in renal kallikrein formation which is normalized by oral kallikrein. The hypotensive action of oral kallikrein as well as its stimulating effects on renal kallikrein release suggest that the kallikrein-kinin system is involved in blood pressure regulation and that impaired renal kallikrein activity may be a factor in the maintenance of essential hypertension.
原发性高血压患者的尿激肽释放酶排泄量（0.48±0.05 EU/24小时）显著低于血压正常的对照组（1.26±0.14 EU/24小时）。口服猪胰激肽释放酶可使降低的尿激肽释放酶恢复正常，并降低动脉血压。通过放射免疫测定法确定，治疗引起的尿激肽释放酶升高是由于内源性酶释放增加所致。有人提出，高血压患者尿激肽释放酶排泄量低反映了肾激肽释放酶生成存在缺陷，口服激肽释放酶可使其恢复正常。口服激肽释放酶的降压作用及其对肾激肽释放酶释放的刺激作用表明，激肽释放酶-激肽系统参与血压调节，肾激肽释放酶活性受损可能是原发性高血压维持的一个因素。
