Yamada K, Watanabe M, Nishikawa T, Mikami K, Shirai K, Tamura Y, Yamamoto M, Kumagai A, Matsuda Y, Moriya H
Endocrinol Jpn. 1978 Dec;25(6):583-9. doi: 10.1507/endocrj1954.25.583.
Urinary kallikrein in a patient with Bartter's syndrome was remarkably higher than normal. Indomethacin treatments increased serum potassium concentration and urinary Na/K ratio, and improved the response of blood pressure to angiotensin II infusion, while it decreased plasma renin activity, plasma aldosterone and urinary kallikrein. The purified urinary kallikrein had one component of the iso-electric point 4.3 by isoelectric focusing using Ampholine system, and its molecular weight was 4.2 x 10(4), which was greater than those of three components of normal human urinary kallikreins (normal HUK). Also Km values with TAME and BAME of urinary kallikrein in our patient with Bartter's syndrome did not correspond to those of normal HUK. Thus it can be said that urinary kallikrein in our patient with Bartter's syndrome was qualitatively different from normal HUK. The present observation might be a reflection of renal tubular dysfunction in this patient with Bartter's syndrome.
巴特综合征患者的尿激肽释放酶显著高于正常水平。吲哚美辛治疗可提高血清钾浓度和尿钠/钾比值,并改善血压对血管紧张素II输注的反应,同时降低血浆肾素活性、血浆醛固酮和尿激肽释放酶。使用两性电解质系统通过等电聚焦法对纯化的尿激肽释放酶进行分析,发现其具有一个等电点为4.3的组分,分子量为4.2×10⁴,大于正常人类尿激肽释放酶(正常HUK)的三个组分。此外,我们这位巴特综合征患者的尿激肽释放酶对甲苯磺酰-L-精氨酸甲酯(TAME)和苄酯-L-精氨酸甲酯(BAME)的米氏常数(Km值)与正常HUK的不同。因此可以说,我们这位巴特综合征患者的尿激肽释放酶在性质上与正常HUK不同。目前的观察结果可能反映了该巴特综合征患者的肾小管功能障碍。