Vinci J M, Gill J R, Bowden R E, Pisano J J, Izzo J L, Radfar N, Taylor A A, Zusman R M, Bartter F C, Keiser H R
J Clin Invest. 1978 Jun;61(6):1671-82. doi: 10.1172/JCI109088.
The kallikrein-kinin system was characterized in seven patients with Bartter's syndrome on constant metabolic regimens before, during, and after treatment with prostaglandin synthetase inhibitors. Patients with Bartter's syndrome had high values for plasma bradykinin, plasma renin activity (PRA), urinary kallikrein, urinary immunoreactive prostaglandin E excretion, and urinary aldosterone; urinary kinins were subnormal and plasma prekallikrein was normal. Treatment with indomethacin or ibuprofen which decreased urinary immunoreactive prostaglandin E excretion by 67%, decreased mean PRA (patients recumbent) from 17.3+/-5.3 (S.E.M.) ng/ml per h to 3.3+/-1.1 ng/ml per h, mean plasma bradykinin (patients recumbent) from 15.4+/-4.4 ng/ml to 3.9+/-0.9 ng/ml, mean urinary kallikrein excretion from 24.8+/-3.2 tosyl-arginine-methyl ester units (TU)/day to 12.4+/-2.0 TU/day, but increased mean urinary kinin excretion from 3.8+/-1.3 mug/day to 8.5+/-2.5 mug/day. Plasma prekallikrein remained unchanged at 1.4 TU/ml. Thus, with prostaglandin synthetase inhibition, values for urinary kallikrein and kinin and plasma bradykinin returned to normal pari passu with changes in PRA, in aldosterone, and in prostaglandin E. The results suggest that, in Bartter's syndrome, prostaglandins mediate the low urinary kinins and the high plasma bradykinin, and that urinary kallikrein, which is aldosterone dependent, does not control kinin excretion. The high plasma bradykinin may be a cause of the pressor hyporesponsiveness to angiotensin II which characterizes the syndrome.
在七名患有巴特综合征且代谢方案恒定的患者中，于使用前列腺素合成酶抑制剂治疗前、治疗期间及治疗后，对激肽释放酶 - 激肽系统进行了特征分析。患有巴特综合征的患者血浆缓激肽、血浆肾素活性（PRA）、尿激肽释放酶、尿免疫反应性前列腺素E排泄量及尿醛固酮水平均较高；尿激肽水平低于正常，血浆前激肽释放酶正常。使用消炎痛或布洛芬治疗使尿免疫反应性前列腺素E排泄量降低67%，使平均PRA（患者卧位时）从每小时17.3±5.3（标准误）ng/ml降至3.3±1.1 ng/ml，平均血浆缓激肽（患者卧位时）从15.4±4.4 ng/ml降至3.9±0.9 ng/ml，平均尿激肽释放酶排泄量从每天24.8±3.2甲苯磺酰精氨酸甲酯单位（TU）降至12.4±2.0 TU，但使平均尿激肽排泄量从每天3.8±1.3μg增至8.5±2.5μg。血浆前激肽释放酶保持不变，为1.4 TU/ml。因此，随着前列腺素合成酶受到抑制，尿激肽释放酶、激肽及血浆缓激肽的值与PRA、醛固酮及前列腺素E的变化同步恢复正常。结果表明，在巴特综合征中，前列腺素介导了低尿激肽和高血浆缓激肽，且依赖醛固酮的尿激肽释放酶并不控制激肽排泄。高血浆缓激肽可能是该综合征所特有的对血管紧张素II升压反应低下的原因。
