Hörl W H, Heidland A
Klin Wochenschr. 1981 Jul 1;59(13):761-3. doi: 10.1007/BF01721264.
Proteolytic activity, with azocasein as substrate in the presence and absence of 0.4 IU kallikrein (Padutin) was measured in the 24 h urine fractions of 100 ambulatory patients with hypertension, proteinuria or haematuria. Urinary protein and alpha 1-antitrypsin concentration have also been assayed. There was an inverse relationship between kallikrein activity and urinary alpha1-antitrypsin concentration( r = 0.84; y = 39.2 e-0.009x). Furthermore, kallikrein activity and 24 h urinary alpha 1-antitrypsin excretion were also inversely correlated (r = 0.81; y = 886,4 e-0.011x). Our data suggest an inactivation of renal kallikrein by urinary alpha 1-antitrypsin.
以偶氮酪蛋白为底物,在有和没有0.4国际单位激肽释放酶(胰激肽原酶)存在的情况下,对100例患有高血压、蛋白尿或血尿的门诊患者的24小时尿液样本进行了蛋白水解活性测定。同时还检测了尿蛋白和α1-抗胰蛋白酶浓度。激肽释放酶活性与尿α1-抗胰蛋白酶浓度呈负相关(r = 0.84;y = 39.2 e-0.009x)。此外,激肽释放酶活性与24小时尿α1-抗胰蛋白酶排泄量也呈负相关(r = 0.81;y = 886.4 e-0.011x)。我们的数据表明,尿α1-抗胰蛋白酶可使肾激肽释放酶失活。